Talking about gastritis & peptic ulcer disease ( definetions , clinical picture , diagnosis & treatment , complications ) , all informations are Up tu date of 2017

1. Gastritis
Peptic Ulcer Disese
DONE BY : AYMAN JADALLAH

2. Gastritis

3. Definetion
 it is the term applied to describe inflammation , erosion , or damage of the
gastric lining that has not developed into an ulcer .

4. Types of Gastritis :
 Type A  its from atrophy of the gastric mucosa & is associated with
autoimmune processes , such as Vit B12 deficiency .Type A is also linked to
diminished gastric acid production & Achlorhydria .
 Type B  can be caused by Alcohol , NSAIDs , H.pylori , head trauma ,
burns & mechanical ventilation . Type B is by far the most common type of
Gastritis . Its also associated with increased Gastric acid production .

5. Clinical presentation
 Patients may be Asymptomatic or may complain of epigastric pain, nausea,
vomiting, hematemesis, or melena.
* There are no unique physical findings for gastritis.

6. Diagnosis
 Only upper endoscopy can definitively diagnose erosive gastritis. Although
anemia may occur, there are no specific blood tests. Radiologic studies
such as an upper gastrointestinal (GI) series will not be specific enough.
 in H pylori infection can be detected by the urease breath test, serum IgG
antibodies (which point to a history of exposure, not current infection), H
pylori stool antigen (indicates current infection), or endoscopic biopsy .

7. Treatment
 Testing for Helicobacter pylori should be performed because this organism should be
treated if it is associated with gastritis.
 Decrease intake of exacerbating agents. Antacids, sucralfate, H2 blockers, and/or PPIs
may help.
 Administer triple therapy (amoxicillin, clarithromycin, omeprazole) to
treat H pylori infection unless the patient is penicillin allergic, in which
case metronidazole should be substituted for amoxicillin.
 Give prophylactic PPIs to patients at risk for stress ulcers (eg, ICU
patients).
 Vit B12 replacement (Atrophic gastritis is associated with vitamin B12 deficiency).

8. Peptic Ulcer Disese

9. Definition
  A disease characterized pathologically by ulceration of the mucosa of
stomach, duodenum and some time of the lower oesophagus or in a
mickle diverticulum. It results when aggressive factors overwhelm
defensive factors involved in mucosal resistance.
  It is characterized clinically by epigastric pain and dyspepsia with
remission and relapses.

10. Etiology & pathophysiology
 Still the precise mechanism of PUD is unclear, but we know that
PUD results when aggressive factors overwhelm defence factors
( mucosal injury-protection balance).
Injurious factors :
 Endogenous
Acid , pepsin, bile acids and small intestine contents.
 Exogenous
Ethanol, Aspirin, NSAIDs, and Helicobacter pylori.
 Protective factors:
Mucus, bicarbonate, mucosal blood flow, prostaglandins, and
Epidermal growth factors .

11. Etiology & pathophysiology
1- Helicobacter pylori associated PUD:
PUD is strongly associated with H.pylori infection
It is a slow-growing gram negative spiral, with multiple
make it motile and allowing it to burrow and live deep
the mucus layer closely adherent to the epithelial surface.
It is protected from gastric acid by the juxta-mucosal mucous
layer which trap bicarbonate secreted by antral cells , and
ammonia produced by bacterial urease.
The mechanism by which HP are involved in pathogenesis
peptic ulcer are unclear, but HP produce ammonia and
toxines that may directly damage the mucosa and initiate an
inflammatory response .
It causally associated with DU because inpatient with DU:
A- 95% are infected with HP in the antrum.
B- Cure of infection heals ulcer and stop ulcer recurrence.

12. Etiology & pathophysiology
2- NSAIDs related PUD :
Aspirin and NSAIDs causes mucosal injury and ulceration of
oesophagus, stomach and duodenum by both direct mucosal
injury and inhibition of prostaglandins that are protective to
the mucosa. Increasing risk for mucosal damage by:
A. History of PUD.
B. High dose of NSAID.
C. Concomitant steroid use.
D. Use of more than one NSAID.
E. Presence of HP infection.

13. 3- Acid related PUD:
Acid appears to be essential for benign peptic
injury to occur . A PH of 1 to 2 maximizes the
activity of pepsin . Furthermore, mucosal
injury from aspirin , NSAIDs, & bile acids is
augmented in the presence of acid .
Etiology & pathophysiology

14. 4- Others :
A- Genetic susceptibility
B- Hypersecretory syndromes
Etiology & pathophysiology

15. 5- Smoking :
A. Smokers are more likely to have PUD.
B. Difficult to heal, longer period of treatment higher dose of drugs,
and refractory.
C. Relapses more and sooner
D. Stop smoking , recurrence as nonsmoker.
Etiology & pathophysiology

16. Clinical presentation
PUD is a chronic condition with a natural history of spontaneous relapse and
remission lasting for decades .
Gus and DUs share common symptoms which are:
1. Abdominal pain - Recurrent
- Epigastric
- Relation to food
2. Vomiting
3. Anorexia and nausea
4. Silent - Anaemia , Haematemesis or perforation.

17. 1.History and Physical examination.
2.Diagnostic studies:
A.Patients under 55 years of age, typical symptoms & HP positive ,
start eradication therapy.
Diagnosis of HP infection:
Noninvasive :
1. Serology sensitive but less specific. Not useful for eradication .
2. Urea breath test high sensitivity 97% and specificity 96%. Very
suitable for testing for eradication.
3. Stool antigen test highly sensitive 98% and specific 96%. Very suitable for
diagnosis & monitoring efficacy of eradication.
Invasive (endoscopy):
1.Biopsy urease test 2.Histology . 3.Culture
B. Patients above 55 years of age, Upper GI Endoscopy & biopsy :
DIAGNOSIS

18. Upper GI Endoscopy & biopsy
The gold standard for the diagnosis of HP infection, beacuase histology not only
confirms the presence of HP ,but also gives information on the presence or absence
of gastritis, gastric atrophy , intestinal metaplasia , MALT lymphoma, and cancer.
Sensetivity & Specificity 95%.
False negative result in:
a.Recent GI bleed.
b.Use of bismuth
c. Use of antibiotics.
d.Use of sucralfate.
e.Use of acid –suppressive therapy .
Accordingly endoscopy is indicated for:
1.Patients above age of 55 years with dyspepsia.
2.Patients with GU.
3.Patients with dyspepsia and alarm symptoms.
DIAGNOSIS

19. 1. Diet:
A. Food
- no rigid restriction on diet.
- small frequent feeding are unnecessary.
B .Drugs and life-stile modification .
- Stop smoking
- Stop aspirin and NSAIDs.
- Restriction of alcohol and coffee.
2. Drug therapy:
TREATMENT

20. A. HP associated PUD :
Current recommendations are that all patients with
duodenal and gastric ulcers should have HP eradication
therapy. Standard eradication therapies are successful in
90% . Regimens used are:
1.First-line eradication therapy
PPI 12 –hourly + Amoxil 1gm + Clarithromycin 500 mg
12-hourly for 7 days.
2.Second-line eradication therapy:
PPI + Bismuth subsalicylate + Metronidazole +Tetracycline
TREATMENT

21. B. NSAIDs – Related PUD:
1. Stop offending drug and start anti-secretory.
2. Give PPI or Prostaglandin E derivative if unable to
stop
NSAIDs.
TREATMENT

22. C. Acid-related PUD :
Here we have a group of patients who are HP negative and not on
NSAIDs . The treatment here is to releave symptoms by controlling
acid secretion. We have a wide variety of anti-secretory drugs .
There is little difference in efficacy among Antacid, H2 antagonist,
Prostaglandin , and Scrulfate. However proton-pump inhibitor offers
advantages in :
1. Acceleration of healing (2weeks)
2. Remarkably safe.
TREATMENT

23. 1. Bleeding
2. Perforation
3. Obstruction
4. Penetration
Complications of peptic ulcer disease

24. Surgery for PUD has decreased because of effective medical
treatment and decline in prevalance of peptic ulcer disease.
However surgery is needed for complications .
Procedures done are:
1. Truncal vagotomy and pyloroplasty.
2. Highly selective vagotomy ( Proximal gastric vagotomy)
3. Billruth l and Billruth ll.
Surgical treatment of PUD