peptic ulcer disease lykhatska g.v.. peptic ulcer disease - is recurrent disease, the main feature...

PEPTIC ULCER PEPTIC ULCER DISEASEDISEASE

Lykhatska G.V.Lykhatska G.V.

Peptic ulcer disease Peptic ulcer disease --

Is recurrent disease, the main feature of which is Is recurrent disease, the main feature of which is the formation of defects (ulcers) of the stomach the formation of defects (ulcers) of the stomach

mucosa and / or duodenal mucosa, which mucosa and / or duodenal mucosa, which penetrates to mucosal layer, submucosa and penetrates to mucosal layer, submucosa and

deeper, unlike erosiondeeper, unlike erosion

Definition

Ulcers may range in size from several millimeters to several centimeters.

Ulcers are delineated from erosions by the depth of penetration; erosions are more superficial and do not involve the muscularis mucosae.

1. Helicobacter pylori

2. NSAIDS

3. Heredity

4. Smoking

5. Association with other diseases or known factors

ETIOLOGY of peptic ulcer disease

Zollinger-Ellison syndrome Zollinger-Ellison syndrome Clinical manifestation hypergastrinaemia caused Clinical manifestation hypergastrinaemia caused gastrynoma: gastrin-producing tumor (1 or more) gastrynoma: gastrin-producing tumor (1 or more) of the pancreas, colon, duodenum , of the pancreas, colon, duodenum , peripancreatic lymph nodes, G-cells of the peripancreatic lymph nodes, G-cells of the gastric mucosa (triangle gastrin)gastric mucosa (triangle gastrin)Spread 2.1 cases / 500 000Spread 2.1 cases / 500 00060-80% of cases - benign60-80% of cases - benign1% of gastroduodenal ulcers1% of gastroduodenal ulcersGastrin> 100ph/ml (N), 500-1000ph/mlGastrin> 100ph/ml (N), 500-1000ph/ml

Helicobacter Helicobacter pyloripylori

It is the most important factor in peptic It is the most important factor in peptic ulcer disease.ulcer disease.

It causes It causes 9090-96-96% % of duodenal ulcers and of duodenal ulcers and 70-80% of gastric ulcers.70-80% of gastric ulcers.

Etiology:Helicobacter pylori infection.

Hyperacidity - eg. zollinger ellison.

Drugs - anti-inflammatory (NSAIDs) & Corticostroids.

Cigarette smoking, Alcohol,

Rapid gastric emptying

Personality and stress

Helicobacter pylori:Most common infection in the world (20%)

10% of men, 4% women develop PUD *

Positive in 70-100% of PUD patients.

H.pylori related disorders:– Chronic gastritis – 90%– Peptic ulcer disease – 95-100%– Gastric carcinoma – 70%– Gastric lymphoma– Reflux Oesophagitis.– Non ulcer dyspepsia

NSAIDSAspirin and other non steroidal anti

inflammatory agents damage the gastric mucosal barrier and are an important etiologic factor in 30% cases of gastric ulcer.

PATHOGENESISPATHOGENESIS

ClassificationI. Phase of disease:-Acute-Uncomplete remission-Remission

II. Course of disease: -mild-moderate- severe.

III. Localization: -stomach-duodenum-stomach + duodenum-gastroeneroanostomosis

IV. Association with Helicibacter pylori:- H. pylori – associated- H. pylori – not associated

V. Complications-Hemorrhage-Perforation -Penetration-Pyloristenosis-Malignancy

Example of diagnosis

Peptic ulcer disease,

acute phase,

mild course,

active ulcer of duodenum,

H. pylori – associated.

CLINICAL AND INSTRUMENTAL SYNDROMES

Pain syndromeDyspeptic syndrome: - nausea

- vomiting- heartburn- eructation- constipation

Asthenic syndromeSyndrome of endoscopic changesSyndrome of roentgenographical changes

CLINICAL FEATURESCLINICAL FEATURES

PAINPAINSite: Site:

EpigastriumEpigastrium

Mendel’s symptom Mendel’s symptom “+”“+”

Character: Burning in character

Radiation: Pain is localised and patient is able to point it with his one finger "pointing sign". If pain is radiating to the back in inter scapular region and not responding to antacids or other anti-ulcer drug, suggests posterior penetration of ulcer into the pancreas.

Time of pain:Soon after eating within 15-30 minutes in gastric ulcer while 2-3 hours after eating in duodenal ulcer that frequently awakens the patient at night.

Relation with food:Patient with gastric ulcer are afraid to eat because it causes pain due to release of acid in response to food. Patients with duodenal ulcer feel pain in empty stomach and get relief after taking food which causes partial neutralization of acid. Then in response to food there is increased acid secretion which causes pain after 2-3 hours. Acid induced pain is believed due to acid stimulation of chemical receptors.

Endoscopy:

Endoscopy is the procedure of choice for diagnosis of peptic ulcer

All patients with gastric ulcer require biopsy initially and the follow up endoscopy and biopsy after 6 weeks of starting therapy, to confirm that the ulcer has healed.

PEPTIC ULCER DISEASEPEPTIC ULCER DISEASE

Severity of course

mild moderate severe

PLAN of INVESTIGATIONSPLAN of INVESTIGATIONS

Total blood countBiochemical analysis Urinanalysis, Diastase of urineCoprogramCoprogramHidden blood in fecesHidden blood in fecesECGEndoscopy+biopsy+ HHistologistologyyDiagnosis of HP infectionDiagnosis of HP infectionX-rayX-rayUSDpH-metry

ENDOSCOPYENDOSCOPY

GGastric ulcer astric ulcer (posterior wall)(posterior wall)

GGastric ulcerastric ulcer (angle of stomach)(angle of stomach)

DDuodenal ulcer uodenal ulcer (anterior wall of d(anterior wall of duodenal uodenal bulb)bulb)

DDuodenal ulcer uodenal ulcer (posterior wall of d(posterior wall of duodenal uodenal bulb)bulb)

DDuodenal ulcer uodenal ulcer (middle part, anterior wall, (middle part, anterior wall, 9-12 mm)9-12 mm)

DDuodenal ulceruodenal ulcer

GASTRIC CANCERGASTRIC CANCER(endoscopy)(endoscopy)

Barium meal (double contrast Barium meal (double contrast technique)technique)

Barium meal is less commonly used now.Barium meal is less commonly used now.

It also reveals gastric and duodenal ulcers. It also reveals gastric and duodenal ulcers.

Upper GI series in which doubleUpper GI series in which doublecontrast (barium and air) is used, showing roundedcontrast (barium and air) is used, showing roundedcollection of barium in an ulcer (arrow) in the duodenalcollection of barium in an ulcer (arrow) in the duodenalbulb of a patient presenting with dyspepsiabulb of a patient presenting with dyspepsia

(uncomplicated duodenal ulcer)(uncomplicated duodenal ulcer)

Diagnosis of HP infectionDiagnosis of HP infection

Non-invasive methodsNon-invasive methods Invasive methodsInvasive methods

- H- Histologistologyy

- Cytology- Cytology

- - rapid urease testrapid urease test-CultureCulture

- - carbon urea breathcarbon urea breath test test-blood antibody test-Stool antigen test

Histology

H. pylori can be detected histologically on biopsy of gastric mucosa obtained at endoscopy and stained with haematoxylin and eosin.

Noninvasive methodNoninvasive methodcarbon urea breath test : Breathing tests with : Breathing tests with labelled 13C (the "gold standard") and 14C labelled 13C (the "gold standard") and 14C carbon atoms "Helik" - testcarbon atoms "Helik" - testSerum (immunological) methods: determination Serum (immunological) methods: determination of serum IgG, IgA; rapid tests using capillary of serum IgG, IgA; rapid tests using capillary blood from immunoprecipitation reactionsblood from immunoprecipitation reactionsMolecular biological methods based on PCR Molecular biological methods based on PCR (material for research: saliva, plaque, urine, (material for research: saliva, plaque, urine, feces)feces)Stool test - definition of Hp antigen in stoolStool test - definition of Hp antigen in stool

Urea breath test with I3C

This is a quick and easy way of detecting the presence of H. pylori by urease production with release of labelled CO2 detected on a mass spectrometer.

This test indicates active infection but is expensive.

COMPLICATIONSCOMPLICATIONS

HemorrhageHemorrhage

PerforationPerforation

PenetrationPenetration

PylorPylorostenosisostenosis

MalignancyMalignancy

PERFORATIONDiagnosis is confirmed if an upright or a lateral decubitus x-ray of the abdomen shows free air under the diaphragm or in the peritoneal cavity, but the diagnosis is not excluded if no air is seen.

Penetration - Penetration - penetration ulcers contiguous penetration ulcers contiguous organ tissues which are its bottom (30-35% of organ tissues which are its bottom (30-35% of

all complications).all complications).

the head of the pancreasthe head of the pancreas

liverliver

gall bladdergall bladder

omentulumomentulum

liver, duodenum ligamentliver, duodenum ligament

Gastric outlet obstruction Symptoms include recurrent large volume vomiting, occurring more frequently at the end of the day and often as late as 6 h after the last meal.

Gastric outlet obstruction

Treatment of PUDTreatment of PUD

ANTIBIOTICS ANTIBIOTICS ((ClarithromycinClarithromycin, , AmoxycillinAmoxycillin) )

ANTISECRETORY DRUGSANTISECRETORY DRUGS::

- - PROTON PUMP INHIBITORSPROTON PUMP INHIBITORS

- - H2 RECEPTOR ANTAGONISTSH2 RECEPTOR ANTAGONISTS

- - ANTACIDSANTACIDS (Almagel, Maalox)(Almagel, Maalox)

GASTROCYTOPROTECTORSGASTROCYTOPROTECTORS

DRUGS, WHICH IMPROVE MOTOR FUNCTION DRUGS, WHICH IMPROVE MOTOR FUNCTION OF STOMACH OF STOMACH (Cerucal, Motilium, Eglonil)(Cerucal, Motilium, Eglonil); ;

SPASMOLYTICSSPASMOLYTICS

PROTON PUMP INHIBITORSPROTON PUMP INHIBITORSThese drugs are also called These drugs are also called H+, K+ ATFase inhibitors. H+, K+ ATFase inhibitors. Compared with H2 receptor Compared with H2 receptor antagonists, proton pump antagonists, proton pump inhibitors provide faster pain inhibitors provide faster pain relief and more rapid ullcer relief and more rapid ullcer healinghealing. . They are the most powerful They are the most powerful inhibitor of gastric secretion inhibitor of gastric secretion yet discovered. yet discovered. They inhibit over They inhibit over 90% 90% of of 24 24 hour acid secretion while H2 hour acid secretion while H2 blocker less than blocker less than 65% 65% in in standard dosages. standard dosages. They are also used in They are also used in combination therapy for combination therapy for eradication of Helicobacter eradication of Helicobacter pyloripylori

DrugsDrugs DosageDosage

OmeprazoleOmeprazole 20 mg20 mg

LansoprazoleLansoprazole 30 mg30 mg

PantoprazolePantoprazole 40 mg40 mg

RabeprazoleRabeprazole 20 mg20 mg

EsomeprazoleEsomeprazole 20 mg20 mg

ANTACIDSANTACIDS (Almagel, Maalox)(Almagel, Maalox)

Antacids promote ulcer healing Antacids promote ulcer healing through stimulation of gastric defense through stimulation of gastric defense mechanism. mechanism. Due to availability of other potent antiDue to availability of other potent anti ulcer ulcer drugs they are not used as first line agents in drugs they are not used as first line agents in the treatment of acute ulcers.the treatment of acute ulcers.

ERADICATION OF H. PYLORI ERADICATION OF H. PYLORI INFECTIONINFECTIONTriple therapyTriple therapy

Amoxycillin 10Amoxycillin 1000mg twice daily 00mg twice daily ++Clarithromycin Clarithromycin 500mg twice daily500mg twice daily + +Proton pump inhibitorProton pump inhibitor (Lansoprazole 30(Lansoprazole 30mg twice dailymg twice daily))

QQuadrupleuadruple therapy therapy Tetracycline 500mg Tetracycline 500mg 4 4 times daily +times daily +

Metronidazole 500mg 4Metronidazole 500mg 4 times daily +times daily +De-nol 120mg De-nol 120mg 4 4 times daily +times daily +Proton pump inhibitorProton pump inhibitor (Lansoprazole 30(Lansoprazole 30mg twice dailymg twice daily))