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?