PUD

Question 1

Peptic ulcer disease

Answer 1

• disturbance in balance between secretion of acid and pepsin by stomach and mucosal barrier (thick layer of mucus)
• Gastric ulcer: decreased resistance of gastric mucosa
• Duodenal ulcer: hyperacidity

Question 2

Pathogenesis of PUD

Answer 2

• invade only mucous membrane
  1. H.pylori
• convert urea using bacterial urease forming ammonium chloride and monochloramine — directly damage epithelial cells — host immune response — inflammatory response — tissue injury
• duodenal ulcer — invade duodenum when gastric metaplasia due to hyperacidity
• produce cytotoxins that possess protease and phospholipase activity— attack and damage mucosal membranes

2. NSAID — inhibit COX — inhibit prostaglandin synthesis which is responsible for production of mucus and bicarbonate which protect stomach mucosa from acid by maintaining alkaline buffer zone
3. smoking
4. alcohol consumption
5. spicy food
6. Zollinger-Ellison syndrome: non insulin secreting islet cell tumour of pancreas produce potent gastrin-like hormone
7. head injury (Cushing’s ulcer)
8. severe burns (Curling’s ulcer)

Question 3

H.pylori related disorders

Answer 3

• chronic gastritis
• PUD
• gastric ca
• gastric lymphoma
• reflux oesophagitis
• non ulcer dyspepsia

Question 4

Gastric ulcer

Answer 4

• lesser curvature
• fibrosis — hour glass contraction of stomach (Kissing ulcer)
• cicatrisation and shortening of lesser curvature — tea-pot deformity (feature of pyloric stenosis, partial gastrectomy with Billroth I anastomosis)
• pain while eating
• relieved by vomiting
• mid epigastric tenderness
• commonly a/w malignancy
• anterior ulcer: tend to perforate
• large chronic ulcer — erode posteriorly into pancreas or major vessels causing internal bleeding

Question 5

Duodenal ulcer

Answer 5

• 1st part of duodenum
• fibrosis — pyloric stenosis
• pain before meal and at middle of night
• cyclical pain
• relieved by taking food, milk
• vomiting is uncommon unless GOO
• duodenal point tenderness
• anterior ulcer: tend to perforate
• posterior ulcer: tend to bleed

Question 6

PE of PUD

Answer 6

• signs of anaemia
• nutritional status
• visible gastric peristalsis

Question 7

Abdominal examination of PUD

Answer 7

• epigastric tenderness
• signs of GOO (visible gastric peristalsis, succussion splash, distended dilated stomach on palpation)
• evidence of gastrointestinal bleeding

Question 8

Blood test of PUD

Answer 8

• FBC: to detect anaemia or infections
• BUSE: to identify electrolytes abnormalities
• fasting serum gastrin: if hypergastrinaemia is suspected–> Zollinger-Ellison syndrome

Question 9

H.pylori Testing

Answer 9

NON INVASIVE
- serological test detect Ig G antibodies

• 13C-urea breath test
  (Patient ingests radioactively labeled Urea (either radioactive carbon-14 or non-radioactive carbon-13). If infection is present, the urease produced by Helicobacter pylori hydrolyzes the urea to form ammonia and labeled bicarbonate that is exhaled as CO2. The labeled CO2 is detected either by a scintillation counter (Carbon-14) and a isotope ratio mass spectrometry or by mass correlation spectrometry (Carbon-13).
  Positive Reaction: Development of an intense magenta to bright pink color in 15 min to 24 h.
  Examples: Proteus spp, Cryptococcus spp, Corynebacterium spp, Helicobacter pylori, Yersinia spp, Brucella spp, etc.

Negative Reaction: No color change.
Examples: Escherichia, Shigella, Salmonella, etc.

• stool antigen test

INVASIVE
- rapid urease test
The test is performed at the time of gastroscopy. A biopsy of mucosa is taken from the antrum of the stomach, and is placed into a medium containing urea and an indicator such as phenol red. The urease produced by H. pylori hydrolyzes urea to ammonia, which raises the pH of the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE).

• Histology
  Giemsa stained sections of gastric mucosa obtained at endoscopy

Question 10

Specific diagnostic

Answer 10

OGDS
- diagnosis and treatment simultaneously

• Forrest classification
  I: active bleeding
  Ia: arterial, spurting haemorrhage
  Ib: oozing haemorrhage

II: stigmata of recent haemorrhage
IIa: visible vessel
IIb: adherent clot
IIc: dark based haematin covered lesion

III: lesion without active bleeding (clean base)

if bleeding PU–> IV pantoprazole infusion 80mg followed by 8mg/ hour (drip infusion up to 72 hours)–> OGDS

• decrease acid secretion from gastric parietal cells by neutralizing gastric acid lead to stabilization of blood clots and stop continuous bleeding ulcer
• continuous infusion: maintain intragastric pH at above 6 to decrease recurrence of continuous bleeding ulcer

Question 11

Imaging test

Answer 11

• erect chest radiograph: to search for gas under diaphragm that signify perforation
• abdominal radiograph: for dilated bowel and air-fluid level that show intestinal obstruction

Question 12

Complication of PUD

Answer 12

Perforation

• anterior wall ulcer
• stomach content into peritoneal cavity — severe pain in epigastric, vomiting, tenderness, guarding — peritoneum secrete lots fluid to neutralize content, last for 6 hours — bacteria from GIT escape causing diffuse peritonitis after 6 hours —septicaemia, oliguria, shock, Hippocratic facies
• Presentation: sudden onset of severe, generalised abdominal pain, abdominal board-like guarding, abdominal movement restricted, patient usually lie still, tachycardia, pyrexia

Bleeding

• posterior wall ulcer
• erode gastroduodenal artery

GOO

• nausea, vomiting, early satiety, ball rolling movement, weight loss
• presence of succussion splash

Question 13

Management of PUD

Answer 13

1. Eradication of H.pylori (Triple therapy)
   - two antibiotics (amoxicillin 1g BD, clarithromycin 500mg BD, metronidazole) and one PPI (omeprazole, pantoprazole 40mg BD) for 10 to 14 days
2. Medical treatment
   - PPI
   - H2 receptor antagonist (ranitidine)
   - antacid (magnesium sulphate and aluminium hydroxide)
   - misoprostol (antagonise NSAID induced PUD)
3. endoscopic treatment
   - Injection (adrenaline, sclerosant, alcohol, pro-coagulant) sclerosant— for oesophageal varices bleeding
   - mechanical (haemostatic clip, band ligation)— for oesophageal varices bleeding
   - thermal (argon plasma, electrocoagulation, heater probe)
4. surgical treatment
   Gastric ulcer
   - body–> partial gastrectomy with Billroth II, antrum –> partial gastrectomy with Billroth I or II combined with Roux-en-Y gastroenterostomy (limit bile reflux) (closure of site of detached afferent loop–> afferent loop is detached and reanastomosed lower down jejunum)

Duodenal ulcer

• truncal vagotomy with either gastrojejunostomy or pyloroplasty : interfere with mechanism of gastric emptying and gastric drainage
• highly selective vagotomy : branches of vagus that supply pyloric sphincter (nerves of Latarjet) are left intact, remaining vagal fibres can be divided without gastric drainage

Question 14

NICE guideline

Answer 14

referral for urgent OGDS

• new-onset dysphagia
• aged >55 years with weight loss and either upper abdominal pain, reflux or dyspepsia
• new onset of dyspepsia not responding to PPI treatment

recommend all identified gastric ulcers are biopsied due to malignant potential and a repeat endoscopy is performed towards the end of PPI therapy to check for resolution