PUD and its causes

1. Peptic Ulcer Disease
Deep Patel - 473

2. Peptic ulcers
-involve ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer).
-Duodenal ulcers are more common.
Common sites
-First part of duodenum
-The lessor curve of the
stomach
-on the stoma following
gastric surgery

3. Causes
H. Pylori bacteria
low income country & settings
gram negative
release protease--->damage mucosa
Starts at antrum--->duodenum
NSAIDs (aspirin and ibuprofen)
1.Inhibit enzyme cyclooxygenase
2.Synthesis of prostaglandins
3.Leaves gastric mucosa susceptible
to damage
Zollinger Ellison syndrome
Tumour- Gastrinoma
NET in duodenal wall or pancreases
Release abnormal Gastrin  parietal cells
release HCL  development of ulcer
Breakdown of the protective layer of the stomach and duodenum
Increase in stomach acid

4. contrast
Duodenal ulcers Gastric ulcers
Incident Resource rich countries, old age, male Resource poor countries, less common than DU, Sex
incidence is equal
Pathology • Common in proximal duodenum
• Penetrate mucosa  mucosal coat 
fibrosis pyloric stenosis
• Ant DU+ Post DU = Kissing ulcer
• Ant DU- tends to perforate/Post DU-
tends to bleed
• rarely seen hourglass contraction of the stomach
• chronic gastric ulcers are much more common on the
lesser curve (the incisura angularis)
• Post erosion may occur – pancreases or splenic artery
, transverse colon(uncommon)
Number/size Small and multiple Large and single
Malignancy uncommon Common, benign chronic GU can transform to
Malignant GU

5. Presentation
eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.
Epigastric pain
often described as gnawing
and may radiate to the back.
normally intermittent rather
than intractable.
Vomiting
it is not a notable
feature unless stenosis
has occurred.
Bleeding
chronic - microcytic
anemia (common) needed
to be investigated with
endoscopy.
Acute- hematemesis and
melaena
Periodicity
Symptoms may disappear for
weeks or months to return
again.

6. investigations
Medical
history
• Regarding steroids and NSAIDs like
• Aspirin
• Ibuprofen
• Naproxen
Physical
examination
• checks for bloating in abdomen
• checking for tenderness or pain
Non-invasive
• Lab test :CBC-Hb-bleeding
• ESR level , CRP
• leucocytosis –inflammation
• campylobacter like org test -dx h. Pylori
• Urea breath test
• gastrin level estimation
• to rule out gastrinomas related ulcers
• Tumour markers
• CEA, CA 19-9
•
Invasive
• Upper endoscopy
• Radiolabelled somatostatin receptor scintigraphy
• ZES angiography- if other dx suspected or GI bleed
• Laparoscopy - both therapeutic and dx
• CT scanning-gastric malignancies

7. Dietary & Life style Modifications
•Eat smaller and more frequent meals
•Eat slowly to allow time to digest
•Stay upright while eating after meals
•Avoid food or drink 2 hours before bedtime
•Avoid the consumption of alcohol
• Stop smoking
• Food and water hygiene
• Eliminate NSAIDs
• Weight loss
• Elevate bed rest
Medical management
1.H2-receptor antagonists and proton pump
inhibitors
2.Eradication therapy
Must given to every patient with PUD
2 antibiotics + 1 PPI
(Amoxicilin+metronidazole+PPI)standard
may not work with
patients with NSAID-associated ulcers
patients with stomal ulceration
patients with Zollinger–Ellison syndrome

8. Surgical management
Duodenal ulcer surgery
• Billroth l
• Billroth II
• Gastrojejunostomy
• Truncal vagotomy
• Highly selective
vagotomy
• Pyroplasty
Gastric ulcer surgery
• Billroth l
• Billroth ll
• Roux-en-Y
Billroth l
Partial/distal gastrectomy
+
Gastroduodenostomy
Billroth ll
Partial/distal gastrectomy
+
Gastrojejunostomy
Truncal vagotomy
(a) division of the anterior vagus (b) mobilisation of the oesophagus (c) division of the posterior vagus.
Highly selective vagotomy
The
anterior
and
posterior
vagus
nerves are
preserved
but all
branches to
the fundus
and body of
the stomach
are divided.
The
anterior
and
posterior
vagus
nerves are
manipulat
ed.

9. COMPLICATIONS PERFORATION IS AN ABNORMAL
CONNECTION THROUGH ALL THREE LAYERS
OF STOMACH OR DUODENUM IN TO
PERITONIAL CAVITY/IT MAY CAUSE
PERITONITIS
CLINICAL FEATURES
• sudden onset severe generalized abdominal pain
• history of peptic ulceration
• stomach are low in bacterial load
• bacterial peritonitis supervenes over a few hours,
• pt. may shocked with tachycardia.
• board like rigidity in abdomen.
• abdomen does not move with respiration.
• pt. unable to move because of pain
• leak from ulcer may not massive..
• right paracolic gutter
Investigations
• Erect plain chest radiograph reveal free gas under
diaphragm
• More accurate CT imaging
• initial priorities are resuscitation and analgesia
• Laparotomy is performed, usually through an upper midline incision if the diagnosis of perforated peptic ulcer can be made with confidence.
• The most important component of the operation is a thorough peritoneal toilet to remove all of the fluid and food debris...
• sufficient tissue is taken in the suture to allow the edges to be approximated, and the sutures should not be tied so tight that they tear out. It is common to place an omental patch over the perforation in the hope of
enhancing the chances of the leak sealing.
• sufficient tissue is taken in the suture to allow the edges to be approximated, and the sutures should not be tied so tight that they tear out. It is common to place an omental patch over the perforation in the hope of
enhancing the chances of the leak sealing.
• When securing the omental patch it is important not to tie the sutures too tight so as to obliterate the omental blood supply.
• distal gastrectomy with Roux-en-Y reconstruction is the procedure of choice.
• All patients should be treated with systemic antibiotics In addition to a thorough peritoneal lavage
Treatment
Bleeding from the ulcer is a common and
potentially life threatening complication.
Population affected has become much older
and the bleeding is commonly associated
with the ingestion of NSAIDs
Diagnosis
can normally be made endoscopically
Treatment
H2-antagonist or a proton pump
antagonist,

10. Thank you