int18 peptic ulcer

7/28/2019 Int18 Peptic Ulcer

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18

Peptic Ulcer

Niazy Abu Farsakh

Saif Rawabdeh

11 / 11 / 2009


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Peptic ulcer disease

It is an ulcer, and this ulcer should be present in an area which has acid and pepsin.

BREAK IN THE GASTROINTESTINAL MUCOSA EXPOSED TO GASTRIC ACID and PEPSINMORE THAN 5 mm in diameter.

MAY BE ACUTE OR CHRONIC.Erosions:

Less than 5 mm in diameter and it is more superficial.

MAY OCCUR IN ACID SECRETING AND NON- ACID SECRETING MUCOSA

PERISTALSIS NOT AFFECTED

HEALS RAPIDLY within 48 hours-3 days

Sites of PUD

It occurs in many sites the commonest are:

1. In the duodenum especialy the first part which we call THE DUODENAL BULB2. In the stomach at the lesser curvature3. Other sites:

a. Lower end of esophagusb. site of gastro -jejunal anastomosis after surgery (It is called Stomal ulcer)c. Opposite to Meckels diverticulm especialy in children

Now, why some patients develop peptic ulcer and others dont?

We have 3 causes for peptic ulcer:

1. HELICOBACTER PYLORI- ASSOCIATED ULCERS

2. NSAIDs

3. HYPERSECRETORY STATES: Zollinger-Elison SYNDROME, IDIOPATHIC.


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Pathogenesis of Peptic Ulcer Disease:

IMBALANCE BETWEEN AGGRESIVE AND DEFENSIVE FACTORS.

AGGRESSIVE FACTORS: Acid and pepsin. (NO ACID AND/OR PEPSIN------NO ULCERATION)

The acid is secreted from the parietal cells of the stomach which are present in the fundus of the stomach, but it isunder control of:

1. Nervous factor2. ENDOCRINOLOGICAL

- Gastrin: Gastrin stimulates acid secretion

3. PARACRINOLOGICAL- GRP: increase secretion of acid

- Somatostatin: decreases secretion of acid

- Histamine : stimulates secretion of acid

What proves that acid has a role in peptic ulcer?

NEVER found when maximum acid output "MAO" is less than 10 mmol/hour RARE when MAO below 20 mmol/h COMMON with higher MAO rates NOT seen when fasting gastric pH is above 2.5. An example of this are patients with achlorhydria never

develop PU. If they have an ulcer then this ulcer may be due to malignancy (Gastric CA).

MAO: Maximum Acid Output. As MAO increases, the possibility that peptic ulcer to occur will increase.

So acid has an essential role in the development of peptic ulcer.

DEFENSIVE FACTORS

PROSTAGLANDINS MUCOSAL BLOOD FLOW: It must be efficient MUCUS GEL LAYER which gives protection against the acid HCO3 which also protects the stomach EPITHELIAL JUNCTIONS are essential so that acid cant go to the epithelial cells REGENERATION OF THE EPITHELIAL LAYER is very important

- GI mucosa has a characteristc feature, it is rapidly regenerating which keeps the cells in a healthy

state.

GROWTH FACTORS: EGF may help to regenerate the GI mucosa

All these factors are essential for the protection against peptic ulcer, and all these defense mechanisms are

mediated by prostaglandins, and thats why when we give patiens NSAIDs these patients are more liable to

develop peptic ulcer.


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Epidemiology of PUD

Prevalence about 5-10% Varies in different communities. Higher prevalence in low socioeconomic classes and with certain diseases. Now we are talking the H-pylori is the main cause of peptic ulcer and H-pylori is present in low socioeconomic classes DU more in males: M/F: 3:1 GU equal in both sexes but increases with age FAMILY HISTORY: 3-4 increased risk . CIGARETTE SMOKING: ulceration increased EMOTIONAL DISTURBANCES and STRESS: increase gastric acid secretion and there will be

decreased blood flow to the stomach.

Thats why patients in the ICU unit or patients with shock or patients with burns are more liable to develop peptic

ulcer.

CLINICAL PICTURE OF PUD:

Symptoms of PUD: Epigastric pain: Localized, dyspepsia may be asymptomatic symptoms related to complications

Signs(On examination): epigastric tenderness signs related to complications

Diagnosis of PUD

Clinical picture is suggestive but not diagnostic Diagnosis best by endoscopy which is the best techni que to diagnose peptic ul cer Barium swallow less helpful no role for serum gastrin or gastric acid studies in usual ulcers, indicated if ZE is suspected Evaluation for H pylori infection Every Gastr ic ul cer shoul d be biopsied to exclude malignancy

While duodenal ulcers have nothing to do with malignancy


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This is how ulcer appears on radiology

And these

are endoscopic views of peptic ulcer.


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And these are erosion

Duodenal ulcer

H-pylori: Flagellated organism produces urease which splits urea into ammonia and CO 2, and ammonia has a

smell.


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Role of H-pylori in GI diseases

Healthy subjects 20-50% Chronic active gastritis 100% Duodenal ulcer >90% Gastric ulcer 50 - 80% Gastric adenocarcinoma 90% Gastric lymphoma 85% MALToma 90%

Diagnosis of Helicobacter pylori infection

Patients with Duodenal peptic ulcer shouldnt be investigated whether they have H-pylori or not because almost all

cases of duodenal ulcer have H-pylori.

Every gastric ulcer should be biopsied to exclude malignancy, so in your way take a specimen and check if it is

H-pylori +ve or not.

Invasive( through endoscopy) Gastric biopsy and staining from the antrum of the stomach, but in order for H-pylori to invade

the duodenum, the duodenal mucosa must be changed to gastric type by metaplasia

culture of biopsy specimen Tests using urease enzyme in biopsy specimens through PH indicator

Non-invasive: Urea breath test: We give the patient urea with radiolabled carbon to drink, then after 30min-1

hour we measure the radiolabled carbon in his breath

H-pylori antibodies not useful Stool antigen Salivary antigen

Complications of Peptic Ulcer Disease

Hemorrhage: The commonest one. 20% of patients with peptic ulcer are liable to bleed, and this bleedingmay lead to death

Perforation may occur in 1% of patients Gastric outlet obstruction due to healing of the ulcer by fibrosis penetration in posterior ulcers in the duodenum


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A bleeding ulcer and we can know that by this red spot

This x-ray shows us air under the diaphragm which indicates ulcer perforation

And this is gastric outlet obstruction


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Natural history of PUD

PUD is a chronic episodic disease with relapses and remissions. If left untreated, 30-40 % of ulcers heal within 8 weeks. Recurrence rate without treatment is 70% during first year and 90% within 2 years. Complications develop in 20% of PUD

The episodic nature of PUD may be related to curtain semesters in the year like Autumn and spring actually we see

most cases of PU in these time.

TREATMENT OF PEPTIC ULCER DISEASE

AIM OF TREATMENT:

- RELIEVE SYMPTOMS- HEAL THE ULCER

- PREVENT COMPLICATIONS

- PREVENT RECURRENCES

A. Life-style modification in PUD

Doubtful efficacy

REST RELAXATION GOOD SLEEP DIET:

bland diet frequent small meals caffeine-containing beverages role of milk fat diet spices alcohol fiber vitamin E and dietary fatty acids


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b. ANTACIDS

Rapid symptomatic relief due to its neutralizing action to the acid Cheap Large amounts are required to heal ulcers leading to undesirable side effects. If taken on empty stomach; they are effective only for 10-20 minutes If taken one hour after meals they are effective for 2-3 hours. Tablet preparations are less effective than suspensions

Side effects of antacids

- Sodium bicarbonates:

increases sodium load: contraindicated in patients with heart failure and/or renal impairment milk- alkali syndrome

- Aluminum compounds:

constipation binds phosphates binds drugs.

- Magnesium compounds:

diarrhea accumulation in renal failure

- Calcium compounds:

constipation rebound hyperacidity

Thats why antacids are usually made in mixture form

C. HISTAMINE- RECEPTOR ANTAGONISTS (H2-Blockers )

CIMETIDINE 400mg RANITIDINE 150mg FAMOTIDINE 20mg NIZATIDINE 150mg


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Act through blocking H2 receptors in the parietal cells Suppress nocturnal acid secretion by more than 90% Suppress 24 hour acid secretion by 50-70% Side effects : somehow very safe drugs

CNS effects: headache, mental confusion Reversible gynecomastia and impotence. Interaction with drugs metabolized through hepatic cytochrome P-450 microsomal enzymes

d. PROTON PUMP INHIBITORS (PPIs): which are the best drugs to suppress the acid

secretion

Suppress acid secretion by non-competitively and irreversibly inhibiting the H+ , K+- ATPase of thegastric parietal cells

Inhibit over 90%of 24-hour acid secretion Increase secretion of gastrin usually 2-3 times the baseline with proliferation and growth of ECL cells No carcinoid tumors reported to occur in man due to PPIs Heal 50% of DUs by 2 weeks, 90% in 4 weeks and almost all by 6-8 weeks and thats why now we dont

have refractory ulcer if the patients takes appropriate amounts of PPI s

Examples:

Omeprazole: 10, 20 mg

lansoprazole: 15, 30 mg pantoprazole: 20, 40 mg rabeprazole: 10, 20 mg esomeprazole:20, 40 mg Tenatoprazole: 40 mg: longer duration of action

New therapies which are present in the slides are still under investigation

e. Eradication therapy for H.Pylori

In vitro HP highly suggestive to many antibiotics In vivo, sensitive to the following agents:

amoxicillin tetracycline clarithromycin


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Metronidazole, tinidazole bismuth PPIs Second line drugs: Levofloxacin, gatifloxacin, rifabutin

- Triple therapy: PPI+ clarithromycin + (amoxicillin or Metronidazole)

- Quadriple therapy: PPI+ bismuth+ tetracycline+ metronidazole

- Both regimens are given for 10 days

- Efficacy of the regimen depends upon drugs used, compliance of patient, resistance pattern of HP in

the area

- Relapse rate drops to less than 10% per year after successful eradication

f. SUCRALFATE

1gm 4 times daily on empty stomach Healing rate: 70-80% within 8 weeks binds with the proteinaceous base of the ulcer forming a coat around the base of the ulcer increasing local mucosal production of PGs Side effects:

constipation nausea reduces the absorption of some drugs binds phosphate in the gut

g. PROSTAGLANDINS

Inhibit gastric acid secretion and has cytoprotective effects They are less effective than H2- blockers side effects:

abdominal cramps diarrhea not cost-effective abortion: and now it is the main use for pgs to induce labor

Indicated for prophylactic use rather than for treatment

h. Surgery for PUD

Rare after introduction of effective therapeutic agents except for complications

Thank you Done by: Saif Aldin naif Rawabdeh (abo naif)

www.sawa2006.com

int18 peptic ulcer

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