peptic ulcer
TRANSCRIPT
Peptic ulcer disease
By Dr. Osman Bukhari
Site: 1- Stomach 2- Duodenum 3- Lower esophagus 4- Jejunum after gastrojejunostomy 5- Terminal ileum adjacent to Mekels diverticulum which contains
ectopic gastric mucosa
Types 1- Acute: superficial 2- Chronic: deep to muscularis mucosa
Fibrosis
Epidemiology 1- Prevalence of PU is 3-4%.
2- 10% of male & 8% of female suffer PU in their lifetime. 3- DU > GU (3:1)
4- Male: Female 4:1-2:1 in DU 2:1 or less in GU
5- Geographical variation. 6- Age DU : 20 50 ـــ years GU : > 40 years
Aeteology 1- H. pylori in 90% with DU & 70%
with GU
2- Acid pepsin VS mucosal barrier - DU occurs in acid hypersecreter. - GU is never found in achlorhydrics e.g pernicious anaemia. **
Severe ulceration occur in Zollenger Ellison syndrome characterized by high acid out put and hyper parathyroidism (Hyperclcaemia stimulates acid secretion)
**Aspirin & NSAID affect the mucosal barrier and may cause GU.
*Bile and intestinal secretions damage gastric mucosal barrier and may cause GU.
3- Smoking depresses gastric mucosal barrier and may cause GU 4- Hereditary : DU is common in blood
group O. FH in DU.
Pathology
1- Break in surface epithelium penetrating
to za muscularis mucosa.
2- Chronic GU are usually single & occur in lesser curvature of antrum in 90%
3- DU more common in the bulb with surrounding duodenitis & 50% occur in the anterior wall
4- DU & GU coexist in 10% 5- 10-15% of DU & 10% of GU are
multiple
Clinical features
1- Natural history is that of remissions and relapses. 2- Epigastric pain - Episodic - Sharply localized - Induced by hunger in DU - Nocturnal & before meal in DU - Relieved by food, milk & anti acids
in DU and by vomiting in GU
3- Anorexia, nausea & weigh loss in GU 4- Heart burn & water brush in DU. 5- Vomiting in 40% . Persistent vomiting
is suspicious of G.L.O obstruction. 6- Persistent pain indicate ulcer
penetration 7- Finger pointing 8- Epigastric tenderness 9- 20-25% are asymptomatic & may
present with complications. e.g. bleeding .
Diagnosis
1- Clinical suspicion 2- Endoscopy is the gold standard
investigation - It is simple, safe & sensitive - Detects associated pathology e.g.
GORD and Ca - GUs biopsed & repeated after
treatment - H. pylori infection is identified in antral biopsies
3- Ba meal +_ double contrast less used now
4- Measurement of gastric acid secretion & serum gastrin levels in Z. Ellison syndrom
5- Ulcer like symptoms in less 40 year do serology or urea breath test for H. pylori and if positive give eradication therapy. Endoscope if symptoms persist after eradication therapy.
6- Ulcer like symptoms for the first time in patients over 40 years should always be endoscoped.
Management of PU Aim of management: a- Relief of pain in short term. b- Induce healing in long term c- Prevent complications * Most ulcers heal in 4-6 weeks * Prevention of relapse needs H. pylori
eradication, maintenance therapy or surgery * H. pylori eradication is the cornerstone of
therapy in PU & successfully prevents relapse and may eliminate the need for long term therapy in the majority of patients.
Short term management1- General managements - Stop smoking. Smoking delays healing,
interferes with H2RA & increase relapse rate
- Stop NSAID (which delay healing, increases relapse rate & complications
- Stop alcohol. - No special diet - Anti acids for symptomatic relief . In
large dose therapy they induce healing in 4-6 weeks
2 - PU associated with H. pylori: - PPI based triple therapy 90%
healing rate & prevents relapse (usually given for 1/52)
- PPI or H2RA often continued for 4-6 weeks to ensure ulcer healing
- If symptoms persist perform urea breath test & if + give further course of eradication using different antibiotics
3 - PU not associated with H. pylori (usually due to NSAID ingestion)
- Withdraw NSAID
- Acid suppression using PPI & H2RA Proton pump inhibitor (PPI) 1- Omeprazole (20mg) 2- Lansoprazole (30mg 3- Pantoprazole (40mg) 4- Esomeprazole (40mg)*PPI has higher ulcer healing rate than
H2RA & better tolerated than misoprostol
but may induce hypergastrinaemia and interact with phenytoin & warfarin
H2 receptor antagonists
1- Cimetidine (200,400 & 800mg tab) 2- Ranitidine (150 & 300mg tab) 3- Famotidine (20 & 40mg tab) 4- Nizatidine (300mg tab) not
recommended for maintenance therapy *Treatment is for 4-6 weeks & is prolonged in smokers, following complication & in patient with GU.
Misoprostol - Synthetic prostaglandin analogue - In low dose used for cytoprotection
in patients on NSAID
- In high dose (200microg×3) it is acid suppression
- Contraindicated in female in child bearing age
- Abdominal pain diarrhoea are the main side effects
Sucralfate - Basic aluminum salt of sucrose
octasulphate - Forms adherent complex with
protiens at ulcer base - Non absorable - Dose 2gm 12 homly
- Dose not suppress acid - Not recommended for long term
therapy
Colloid bismuth - It is tripotassium dicitiato bismuthate - It binds with protiens in ulcer base in
acid PH - Effective agent against H. pylori
- Not recommended for maintenance therapy
- Dose 240mg ×2*Pirenzepine: antimuscarinic.
*Carbenoxolone: leads to HT & Na retention & no longer used.
Long term management of PU: - Continuous long term therapy is not
necessary in the majority of patients after successful H. pylori eradication
- Further management will depend on a- Age of patient b- Rate of relapse c- Occurrence of complications d- Presence of other serous medical disease.
1- Intermittent treatment: if relapses are less than 4 per year
2 - Maintenance treatment: 80% will remain in remission as long as treatment is maintained. It is given for:
a- Frequent relapse interfering with quality of life
b- History of life thertening complication c- In elderly
d- patient with serous medical disease when the risk of future complications
or surgery must be avoided 3- Surgery:- with recent advance in
medical treatment surgery is rarely necessary except for complications.
Surgery can relieve symptoms and prevent complications
Indications for surgery 1- Complication of PU 2- Recurrent ulcer after surgery 3- Failure to comply with medical
TR.
4- Failure of medical therapy specially in young with FH of PU.
5- Previous complications 6- Relapse while on medical
treatment Types of surgery 1- Bill Roth in GU 2- Vagotomy & drainage
procedure in DU
Complications of PU Bleeding (15-20%)
- Present with haematemesis & melaena
- Amount of blood lost is assessed - Hb% is not a good indicator of acute bleeding. - All patients with significant bleeding
within the previous 48 hours should be admitted
- Bleeding stops within 48 hours in 85% of patients
Factors affecting managing: 1- Age 2- Amount of blood loss 3- Shock 4- Evidence of chronic liver disease or
other co morbidities.
- Immediate management A- Urgent resuscitation in shocked patients
1- I.V. canulae 2-Take blood for grouping & cross
matching, Hb, urea, electrolytes & liver biochemistry 3- Assess the patients & monitor pulse & BP frequently
4- Rapid restoration of blood volume
Guide lines for BT 1- Clinical shock 2- PR >100 3- SBP >100 4- Hb <10gm/dl in patients with
active bleeding or recent bleedBlood volume is restored: 1- Initially with volume expanders 2- blood transfusion as soon as possible. 3- avoid overload by using CVP line
B- Urgent endoscopy after resuscitation in patient with shock patients, liver disease or continuing bleeding
- If there is bleeding ulcer: a- Inject adrenaline or sclerosing agent b- Heat, laser or argon coagulation c- If bleeding is uncontrolled ligate the
bleeding artery surgically. * Mortality in bleeding PU is 10-15%. More in elderly.
Perforation - More in DU than GU - May be precipitated by NSAID - Incidence decreased with better
medical care -There may be a history of PU or
perforation may be the first presentation of PU
- Gastric contents lead to peritonitis - There is severe Abdomenal pain &
vomiting.
- Signs of peritonitis - Shock - Decreased liver dullness - Gas under the diaphragm on
radiology is diagnostic - Exclude other causes of acute
abdomen
Management 1- Admission 2- Nil by mouth.
3- N-G suction 4- I.V.fluids 5- Anti biotics 6- Surgery:- drainage, oversewing
+/- vagotomy.
Gastric out flow obstruction
( Pyloric stenosis)
Due to:- a- Fibrosis of DU b- Edema & spasm of active ulcer Diff. Diagnosis a- Ca antrum b- External pressure c- gastro paresis d- Adult hypertrophic pyloric stenosis
Clinical feature & management
1- Long history of DU 2- Persistent vomiting - Large & projectile - Contain previous food elements 3- Epigastric fullness, visible
peristalsis and succussion splash 4- Dehydration & electrolyte
disturbances 5- Metabolic alkalosis and tetany.
6- Wasting & malnutrition. 7- High fasting gastric juice 8- Ba meal rarely advised (gastro
graffin) 9- Endoscopy 10 - Correct fluid & electrolytes
disturbance and improve nutrition Treatment opntions include balloon
dilation +_stenting, but surgery with drainage procedure is usually the final answer.
Zollinger Ellison syndrome Triad of: 1- Gastrinoma (non beta cell islet tumour
of pancreas) 2- Gastric acid hypersecretion
3- severe peptic ulceration - 0.1% of cases of PU
- age 30-50y. *Gastrinoma stimulates parietal cells to
max and increases parietal cell mass. *Acid reaches small bowel & lowers PH
inactivating lipase& precipitating bile acids leading to diarrhoea & steatorrhoea.
Pathology - 90% of tum. in head of panc.%.
- 50% multiple - 1/2-2/3 are slow growing malig. tumours - 20-60% have MEA1
Clinically: history is usually short.
- PUs are severe, multiple, recurrent & at unusual sites, poor response to standard ulcer therapy & more complications
- Diarrhoea in 1/3.
Diagnosis Suspected in pat. with severe PU,
specially if Ba.shows abn. coarse gastric folds.
- Gastric acid studies show high basal acid output little affected by pentagastrin - Grossly elevated ser. gastrin confirms the diag. -Tum. localised by CT, E- US and scanning after Octreotide taken by the tumour.
Management - 30% of tum. are small & single and
resectable ( curable). Many are multifocal and some present with metastasis & surgery is inappropriate.
- Higher doses of PPI to suppress sympt - Octreotide s/c reduces gastrin secretion
and is useful. - 5 year survival is 60-80% - Pats die of malig tum rather than PU if if the tum is not resectable - All patients should be monitored for later
development of MEA1.
Problem 1: Epigastric pain - Ali is a 40 years old business man who used
to smoke heavily & drink alcohol regularly for the last 15 years. He was seen by za MO in
medical out patient dept. with periodic epigastric pain for 3years. As he said, za pain is
burning in character & used to awake him in za early hours of za morning & relieved by drinking milk. Ali recalls an episode of haematemesis and melaena 2 years ago.
- Clinical examination was normal a part from
marked epigastric tenderness. The Dr. made
a provisional diagn & requested an investigation
for definite diagnosis
Q1: What was za provisional diagn?
Q2: What was za investigation requested ?
Q3: Discuss za aetiology & pathogenesis of this
disease?
- Ali reported next day wz severe epigastric pain
which started at 8 oo a.m & in due time
became generalized wz persistent vomiting .
- On exam. Ali was in severe pain & shocked. The abdomen was rigid & silent on auscultation.
CXR in za erect position explained Ali,s problem.
Q4: What complication happened to Ali?
Q5: What was the diagnostic X- ray finding?
Q6: Mention 3 differential diagn?
Q7: What za immediate line of management?
- Ali was taken to za theatre after za initial
management for definite TR & had a successful
recovery from za surgery.
Q8: What surgical operation had been done
Ali?
- Ali was discharged from za surgical ward and
referred to za physician for specific TR of the
original disease.
Q9: What are za components of this disease?
Q10: What advice will you offer to Ali concerning
life style modification?