6-GIT lecture about peptic ulcer (continue).ppt

PEPTIC ULCER DISEAES
( CONTINUE )
DR JABBAR JASIM

COMMON SIDE-EFFECTS OF H. PYLORI ERADICATION
THERAPY
1. Diarrhea
 30-50% of patients; usually mild but
Clostridium difficile-associated colitis can
occur
.
2. Flushing and vomiting when taken
with alcohol (metronizadole).
3. Nausea, vomiting.
4. Abdominal cramp.
5. Headache .
6. Rash.

Testing to ascertain H. pylori status after
therapy is indicated in patients with:-
1. Prior complicated ulcer disease.
2. Persistent or recurrent symptoms
after therapy.
3. Patients who fail to complete the
therapeutic course.

 Ascertainment of therapeutic efficacy must be
delayed until at least 1 month after the end of
treatment to prevent false-negative results
related to the temporary suppression but not
eradication of the organism.
 When H. pylori persists, ulcers recur in 50 to
90% of patients within 12 to 24 months, this
rate can be reduced to 20 to 30% with
maintenance acid suppression.

General measures
Cigarette smoking, aspirin and NSAIDs
should be avoided .
 no special dietary advice is required .
Maintenance treatment
Continuous maintenance treatment should not be
necessary after successful H. pylori eradication. For
the minority who do require it, the lowest effective
dose should be used.
 Surgical treatment:-
 elective surgery for peptic ulcer disease a
rarely used because most of peptic ulcer disease
are cure by H pylori eradication &availability
of potent acid suppression therapy .

Indication for surgery in peptic ulcer:-
A) emergency
1)perforation.
2)Hemorrhage (if not stopped after conservative
& endoscopic intervention) .
B) Elective
1) Complications, e.g. gastric outflow
obstruction.
2) Recurrent ulcer following gastric surgery

Type of surgery is partial gastrectomy,
preferably with a Billroth I anastomosis in
which the ulcer itself and the ulcer-bearing
area of the stomach are resected ,the reason
for this is to exclude an underlying cancer
In the presence of giant duodenal ulcers
partial gastrectomy using a Billroth II
reconstruction may be required
.

Complications of gastric resection or
vagotomy :-
In most, the effects are minor but in 10% of cases they
significantly impair quality of life.
1.Dumping:- Rapid gastric emptying leads to distension
of the proximal small intestine as the hypertonic
contents draw fluid into the lumen. Autonomic reflexes
release a range of gastrointestinal hormones which lead
to vasomotor features such as flushing, palpitations,
sweating, tachycardia and hypotension
Patients should therefore avoid large meals with high
carbohydrate content.
2.Bile reflux gastritis leads to chronic gastritis,
treatment with aluminium-containing antacids or
sucralfate may be effective.

3- Diarrhoea and maldigestion:
occurs 1-2 hours after eating.
Factors that may lead to malabsorption.
1)Poor mixing of food in the stomach, with
Rapid emptying,
2)Inadequate mixing with pancreatic biliary
secretions,
3)Reduced small intestinal transit times and
4)Bacterial overgrowth,
Treatment with
1.Dietary advice to eat small, Dry meals with a
2.Reduced intake of refined carbohydrates,
3.Antidiarrheal drugs such as codeine phosphate
(15-30 mg 4-6 times a day) or loperamide (2 mg
after each loose stool) are helpful.

4)Weight loss
because of a small gastric remnant
5)Anaemia
Inadequate dietary intake of iron and folate, lack of acid
and intrinsic factor secretion, mild chronic low-grade
blood loss from the gastric remnant and recurrent
ulceration are responsible.
6)Metabolic bone disease
(osteoporosis and osteomalacia )due to calcium
and vitamin D malabsorption.
7)Gastric cancer:-
risk is highest in those with hypochlorhydria,
duodenogastric reflux of bile, smoking and H. pylori
infection.
Although the relative risk is increased, the absolute risk of
cancer remains low and endoscopic surveillance is not
indicated following gastric surgery.

1- Perforation:
 Perforation occurs more commonly in duodenal than
in gastric ulcers, and is usually found with ulcers on
the anterior wall.
 it cause acute abdomen, after resuscitation, the
acute perforation is treated surgically, either by
simple closure, or by converting the perforation into
a pyloroplasty if it is large.
 Following surgery H. pylori should be treated (if
present) and NSAIDs avoided.
2- Bleeding.
Complications of peptic ulcer disease

Examination
 frequently shows evidence of wasting and dehydration.
 A succussion splash may be elicited 4 hours or more
after the last meal or drink.
 Visible gastric peristalsis is diagnostic of gastric outlet
obstruction.
LAB . TESTS
 low serum chloride and potassium, and raised serum
bicarbonate and urea concentrations.
 This results in enhanced renal absorption of Na+ in
exchange for H+ and paradoxical aciduria.
3- Gastric outlet obstruction
Nausea, vomiting and abdominal distension are the cardinal
features of gastric outlet obstruction. food eaten 24 hours or more
previously may be recognized.

Nasogastric aspiration of at least 200 ml
of fluid from the stomach after an
overnight fast suggests the diagnosis.
Endoscopy should be performed after the
stomach has been emptied by a wide-bore
nasogastric tube.
 Endoscopic balloon dilatation of benign
stenosis may be possible in some patients.

DIFFERENTIAL DIAGNOSIS AND MANAGEMENT OF GASTRIC
OUTLET OBSTRUCTION
Causes Management
1.Fibrotic stricture from duodenal ulcer Balloon
dilatation or surgery
( i.e. 'pyloric stenosis)
2.Oedema from pyloric channel or PPI therapy
duodenal ulcer
3.Carcinoma of antrum Surgery
4.Adult hypertrophic pyloric stenosis Surgery

Management of gastric outlet obstruction
A. Nasogastric suction and intravenous correction of
dehydration are undertaken. In severe cases at least 4
liters of isotonic saline and 80 mmol of potassium may
be necessary during the first 24 hours.
B. Correction of metabolic alkalosis is not required.
C. In some patients proton pump inhibitor drugs heal
ulcers, relieve pyloric oedema and overcome the need
for surgery.
D. In others partial gastrectomy is necessary although this
is best done after a 7-day period of nasogastric
aspiration which enables the stomach to return to
normal size.
E. A gastroenterostomy is an alternative operation but,
unless this is accompanied by vagotomy, patients will
require long-term proton pump inhibitor therapy to
prevent stomal ulceration.

ZOLLINGER-ELLISON SYNDROME
 This is a rare disorder accounts for about 0.1%
of all cases of duodenal ulceration, occurs in
either sex at any age although it is most
common between 30 and 50 years of age.
 It characterized by the triad of severe peptic
ulceration, gastric acid hypersecretion and a
non-beta cell islet tumour of the pancreas
('gastrinoma’)
 About 90% of tumors occur in the pancreatic
head or proximal duodenal wall. Adenomas of
the parathyroid and pituitary glands (multiple
endocrine neoplasia, MEN typeI present in 20-
60% of patients.

 Gastrinoma secretes large amounts of gastrin,
which stimulates the parietal cells of the
stomach to secrete acid to their maximal
capacity and increases the parietal cell mass
three- to six fold.
 The acid output may be so great that it reaches
the upper small intestine, reducing the luminal
pH to 2 or less.
 Pancreatic lipase is inactivated and bile acids
are precipitated.
 Diarrhoea and steatorrhoea result.

Clinical features:-
Peptic ulcers are multiple, severe and may
occur in unusual sites such as the post-bulbar
duodenum, jejunum or oesophagus.
There is a poor response to standard ulcer
therapy. The history is usually short; bleeding
and perforations are common
Diagnosis should be suspected in all patients
with unusual or severe peptic ulceration,
especially if a barium meal shows abnormally
coarse gastric mucosal folds.

Investigations
1
)
Hypersecretion of acid under basal conditions with little
increase following pentagastrin may be confirmed by gastric
aspiration
.
2
)
Serum gastrin levels are grossly elevated (10- to 1000-
fold)
.
3
)
Injection of the hormone secretin normally causes no
change or a slight decrease in circulating gastrin
concentrations, but in Zollinger-Ellison syndrome produces
a paradoxical and dramatic increase in gastrin
.
4
)
Tumour localisation is best achieved by endoscopic
ultrasound and radio-labelled somatostatin receptor
scintigraphy

Hormone Origin Stimulus Action
Secretin
Duodenum and
jejunum (S cells)
Duodenal
acid
Fatty
acids
1
)
Stimulates
pancreatic fluid
and bicarbonate
secretion
2)Decreases acid
secretion
Reduces gastric
emptying
Origin & action of Secretin hormon

Treatment
 up to 30% of small and single tumors can be localized and
resected ,otherwise high dose PPI heals ulcers and alleviates
Diarrhoea.
Synthetic somatostatin analogue, octreotide, given by
subcutaneous injection, reduces gastrin secretion and is
sometimes of value.
Prognosis 5-year survival is 60-75% and all patients should
be monitored for the later development of other
manifestations of MEN I.

Drugs used in treatment of PU
Drug Type/Mechanism Examples Dose
Acid-suppressing drugs
Antacids Mylanta, Maalox, Tums,
Gaviscon
100–140 meq/L 1 and 3 h after meals and
hs
H2 receptor antagonists Cimetidine
Ranitidine
Famotidine
Nizatidine
400 mg bid
300 mg hs
40 mg hs
300 mg hs
Proton pump inhibitors Omeprazole
Lansoprazole
Rabeprazole
Pantoprazole
Esomeprazole
20 mg/d
30 mg/d
20 mg/d
40 mg/d
20 mg/d
Mucosal protective agents
Sucralfate Sucralfate 1 g qid
Prostaglandin analogue Misoprostol 200 g qid
Bismuth-containing compounds Bismuth subsalicylate
(BSS)
anti-H. pylori regimens

1. Gastric carcinoma .
2. Gastric lymphoma.
3. Gastrointestinal stromal cell tumors (GIST).
4. Gastric carcinoid tumors.
5. Hyperplastic polyps, Adenomatous polyps.

Gastric carcinoma
is more common in men and the incidence rises sharply after 50
years of age
.
• Etiology
1. H. pylori is associated with chronic atrophic gastritis and
gastric cancer ,
2. H. pylori responsible for 60-70% especially if acquiring
infection early in life.
3. Although the majority of H. pylori-infected individuals have
normal or increased acid secretion, a few become hypo- or
achlorhydric and these people are thought to be at greatest
risk.
4. Chronic inflammation with generation of reactive oxygen
species and depletion of the normally abundant antioxidant
ascorbic acid are also important.

Risk factors for gastric cancer
1) H. pylori.
2) Smoking.
3) Alcohol.
4) Dietary associations (Diets lacking fresh fruit and vegetables as well
as vitamins C and A)
5) Autoimmune gastritis (pernicious anemia).
6) Adenomatous gastric polyps.
7) Previous partial gastrectomy (> 20 years).
8) Ménétrier's disease.
9) Hereditary diffuse gastric cancer families (HDC-1
mutations). autosomal dominant trait.
10)Familial adenomatous polyposis (FAP).

Pathology
all tumours are adenocarcinomas arising from mucus-secreting
cells in the base of the gastric crypts
.
 According to cells origin of cancer it is of types:-
A. Intestinal arising from areas of intestinal metaplasia with
histological features reminiscent of intestinal epithelium. This is
more common.
B. Diffuse arising from normal gastric mucosa (poorly differentiated
and occur in younger patients).
Distribution within stomach
1) About 50% of gastric cancers develop in the antrum.
2) 20-30% occur in the gastric body, often on the greater curve.
3) 20% are found in the cardia.
Early gastric cancer is defined as cancer confined to the
mucosa or submucosa, regardless of lymph node involvement.

Diagnosis and staging
• General investigation :
– low Hb, raised ESR, & abnormal liver function which indicate
hepatic metastasis.
• Endoscopy
– is the investigation of choice and should be performed promptly in
any dyspeptic patient with 'alarm features. Barium meal is a poor
alternative.
 Once the diagnosis is made imaging is necessary for accurate staging
and assessment of resectability.
 CT may not demonstrate small involved lymph nodes, but will show
evidence of intra-abdominal spread or liver metastases
 laparoscopy is required to determine whether the tumour is resectable
as it is the only modality that will reliably detect peritoneal spread.

Management
Surgery
– resection offers the only hope of cure, which can be achieved in
90% of patients with early gastric cancer.
– There is no current evidence to suggest that either
neoadjuvant chemotherapy (before surgery and based on 5-
fluorouracil) or adjuvant chemotherapy (after surgery)
improves survival rates and post-operative radiotherapy has
no value.
– Unresectable tumors palliation of symptoms can be achieved
in some patients with:-
1. Chemotherapy
2. Endoscopic laser ablation of tumor tissue for control of
dysphagia or recurrent bleeding.
3. Endoscopic dilatation, laser therapy or insertion of
expandable metallic stents may require for carcinomas at the
cardia to allow adequate swallowing

Prognosis
Overall prognosis remains very poor, with less than 30% surviving 5 years. The
best hope for improved survival lies in greater detection of tumours at an earlier
stage
 Gastric lymphoma
 represent less than 5% of all gastric malignancies. Stomach is
the most common site for extra nodal non-Hodgkin's
lymphoma.
 H. pylori infection is closely associated with the development
of a low-grade lymphoma ('MALToma'). Superficial
MALTomas may be cured by H. pylori eradication.
clinical presentation is similar to that of gastric cancer.
• Treatment
1) low-grade MALTomas consists of H. pylori eradication and
close observation.
2) High-grade B-cell lymphomas are treated by a combination
of chemotherapy, surgery and radiotherapy.

Prognosis :-
favorable prognosis depend on
1. STAGE AT DIAGNOSIS ARE STAGE I
OR II DISEASE
2. SMALL RESECTABLE TUMOURS.
3. TUMOURS WITH LOW-GRADE
HISTOLOGY
4. AGE BELOW 60 YEARS.

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