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Peptic Ulcer Disease( PUD):

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Times New Roman Arial Monotype Sorts Wingdings Notebook 1_Notebook Peptic Ulcer Disease( PUD): Introduction: GASTRIC & DUODENAL ULCER : Aetiology: Aetiology ... – PowerPoint PPT presentation

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Title: Peptic Ulcer Disease( PUD):


1
Peptic Ulcer Disease( PUD)
  • .

2
Introduction
  • Discontinuation of the mucous membrane of the
    GIT.
  • Acute or chronic both penetrate the muscularis
    mucosae but in acute ulcer no evidence of
    fibrosis.
  • Erosions do not penetrate the muscularis
    mucosae.
  • Locations duodenum, stomach, lower oesophagus,
    or in the jejunum after Gastrojejunostomy or,
    rarely, in the ileum adjacent to a Meckel's
    diverticulum.

3
GASTRIC DUODENAL ULCER
  • The prevalence is decreasing in Western
    communities as a result of widespread H. pylori
    eradication, but high in developing countries.
  • Male/female for DU 51-21, for GU is 21 or
    less.

4
Aetiology
  • H Pylori.
  • NSAIDs.
  • Smoking.
  • Genetics.

5
Aetiology H pylori
  • The most important cause.
  • HP prevalence rises with age, 50 gt 50 years are
    infected.
  • In developing world HP is much more common,
    usually acquired in childhood up to 90 of the
    adults are infected.
  • The vast majority of colonised people remain
    healthy/ asymptomatic only a minority develop
    clinical disease.
  • 90 DU, 70 GU are infected with H. pylori the
    remaining 30 GU are due to NSAIDs.

6
H pylori Pathophysio
  • H. pylori is Gram-negative, spiral with multiple
    flagella at one end which make it motile,
    allowing it to burrow live deep beneath the
    mucus layer closely adherent to the epithelial
    surface.
  • It uses an adhesin molecule (BabA) to bind to
    the Lewis b antigen on epithelial cells,where the
    surface pH is close to neutral any acidity is
    buffered by the organism's production of the
    enzyme urease.produces ammonia from urea, raises
    the pH around the bacterium between its two
    cell membrane layers.
  • The bacteria spread by person-to-person contact
    via gastric refluxate or vomitus.
  • H. pylori exclusively colonises gastric-type
    epithelium found in the duodenum only in
    association if there are patches of gastric
    metaplasia.

7
H pylori Pathophysio
  • Causes chronic gastritis by provoking a local
    inflammatory response in the underlying
    epithelium, depends on numerous factors
    bacterial factors as expresion of cagA / vacA
    genes host factors.

8
H pylori Pathophysio
  • Bacterial factots
  • H. pylori strains expressing cagA (cagA) are
    more often associated with disease than cagA-
    strains.
  • Most strains also secrete a large pore-forming
    protein called vacA causes large vacuoles to form
    in cells in vitro.

9
H pylori Pathophysio
  • Host factors
  • Genetic polymorphisms for example, greater
    levels of expression of the proinflammatory
    cytokine interleukin-1ß (IL-1ß) are associated
    with greater risk of gastric atrophy subsequent
    carcinoma polymorphisms in other genes involved
    in the host inflammatory response to infection
    (e.g. IL-10 / TNF-a) may also be important.

10
H pylori Pathophysio
  • In most people H. pylori causes antral gastritis
    associated with depletion of somatostatin (from D
    cells) gastrin release from G cells unchecked by
    somatostatin.
  • The subsequent hypergastrinaemia stimulates acid
    production by parietal cells, but in the majority
    of cases this has no clinical consequences.
  • In a minority of patients (perhaps smokers) this
    effect is exaggerated, leading to duodenal
    ulceration
  • The role of H. pylori in the pathogenesis of
    gastric ulcer is less clear but probably acts by
    reducing gastric mucosal resistance to attack
    from acid/pepsin.
  • In 1 of infected people, H. pylori causes a
    pangastritis leading to gastric atrophy/
    hypochlorhydria,allows bacteria to proliferate
    within the stomach these may produce mutagenic
    nitrites from dietary nitrates, predisposing to
    the development of gastric cancer

11
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13
Factors which influence the virulence of H.
pylori.
14
HP Diagnosis
  • Urea Breath tests are best because of their
    accuracy, simplicity non-invasiveness.

15
HP Diagnosis Others
Test Advantages Disadvantages
NON-INVASIVE NON-INVASIVE NON-INVASIVE
Serology Rapid office kits available Lacks sensitivity and specificity
  Good for population studies Cannot differentiate current from past infection
Urea breath tests High sensitivity and specificity 14C uses radioactivity
    13C requires expensive mass spectrometer
Faecal antigen test Cheap, accurate Acceptability
INVASIVE (ANTRAL BIOPSY) INVASIVE (ANTRAL BIOPSY) INVASIVE (ANTRAL BIOPSY)
Histology Sensitivity and specificity False negatives occur
    Takes several days to process
Rapid urease tests, e.g. CLO, Pyloritek Cheap, quickSpecificity Lack sensitivity
Microbiological culture 'Gold standard' Slow / laborious
  Defines antibiotic sensitivity Lacks sensitivity
16
Smoking
  • Smoking confers an increased risk of gastric
    ulcer to a lesser extent, duodenal ulcer.
  • Once the ulcer has formed, it is more likely to
    cause complications less likely to heal if the
    patient continues to smoke.
  • NSAIDs

17
Acid-pepsin vs mucosal resistance
  • Ulcer forms when there is imbalance between
    aggressive factors, i.e. acid /pepsin defensive
    factors, i.e. gastric /duodenal mucosa,
    bicarbonte, mucosal blood flow PGs.
  • Ulcers occur only in the presence of acid
    /pepsin never found in achlorhydric as
    pernicious anaemia severe intractable PU nearly
    always occurs in ZES, characterised by very high
    acid secretion.
  • Most DU have markedly exaggerated acid secretion
    in response to stimulation by gastrin H. pylori
    leads to hypergastrinaemia.
  • In GU the effects of H. pylori are more
    compleximpaired mucosal defence resulting from a
    combination of HP, NSAIDssmoking have a more
    important role.

18
Gastroduodenal mucosal protection PG stimulate
HCO3 /mucus secretion increase mucosal blood
flow.
19
Clinical features
  • Chronic with spontaneous relapse /remission
    lasting for decades, if not for life.
  • DU/GU share common symptoms.
  • Recurrent abd pain with 3 notable
    characteristics epigastric , episodic
    relationship to food .
  • Occasional vomiting occurs in 40 persistent
    daily vomiting suggests GOO.
  • In 1/3 history is less characteristic, esp in
    elderly on NSAIDs, pain may be absent or slight
    epigastric unease.
  • Occasionally, only anorexia / nausea, or a sense
    of undue repletion after meals.
  • In some completely 'silent', presenting for the
    first time with anaemia, abrupt haematemesis or
    as acute perforation recurrent acute bleeding.
  • The diagnostic value of individual symptoms is
    poor.

20
Diagnosis
  • Endoscopy is the preferred investigation.
  • Gastric ulcers may occasionally be malignant
    therefore must always be biopsied followed up
    to ensure healing

21
Management
  • Aims relieve symptoms, induce healing ,prevent
    recurrence.
  • H. pylori eradication is the cornerstone of
    therapy, as this will successfully prevent
    relapse eliminate the need for long-term therapy
    in the majority.
  • H. pylori eradication All patients with proven
    acute or chronic DU GU who are H.
    pylori-positive should be offered eradication as
    primary therapy.
  • Treatment is PPI simultaneously with two
    antibiotics (from amoxicillin, clarithromycin ,
    metronidazole) for 7 days.
  • Success is gt 90, although compliance,
    side-effects metronidazole resistance influence
    the success of therapy.
  • Second-line therapy should be offered to those
    patients who remain infected after initial
    therapy,choice lies between a third attempt with
    quadruple therapy (bismuth, PPI 2 antibiotics)
    or long-term maintenance therapy with PPI.

22
Management
  • H. pylori / NSAIDs are independent risk factors
    for ulcer
  • High risk patients requiring long-term NSAIDs
    should first undergo eradication therapy to
    reduce ulcer risk.
  • This may not be necessary in young, fit patients
    with no history of ulcer disease or dyspepsia but
    a 'test treat' strategy for older patients with
    major comorbidity or a previous ulcer history is
    recommended.
  • Subsequent co-prescription of PPI NSAID is
    advised but is not always necessary for patients
    being given low-dose aspirin in whom the risk of
    ulcer complications is lower

23
COMMON SIDE-EFFECTS OF HP ERADICATION
  • Diarrhoea
  • 30-50 usually mild but Clostridium
    difficile-associated colitis can occur.
  • Flushing vomiting when taken with alcohol
    (metronizadole)
  • Nausea, vomiting
  • Abdominal cramp
  • Headache
  • Rash

24
Other indications OF HP ERADICATION
  • Definite
  • Peptic ulcer
  • MALToma
  • H. pylori-positive dyspepsia
  • Not indicated
  • Asymptomatic
  • Gastro-oesophageal reflux disease
  • Uncertain
  • Family history of gastric cancer
  • Non-ulcer dyspepsia
  • Low risk Long-term NSAID users

25
General measures
  • Cigarette smoking, aspirin/ NSAIDs should be
    avoided.
  • Alcohol in moderation is not harmful.
  • No special dietary advice is required.
  • Short-term management many different drugs are
    available for of acid peptic symptoms.
  • 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.

26
Group Examples Mechanism Comments
antacid Aluminium hydroxide, magnesium trisilicate, alginic acid Antacids alginates form protective mucosal 'raft' Aluminium salts block digoxin absorption and are constipating while magnesium salts can cause diarrhoea some have high sodium content and can exacerbate cardiac failure
H2-Bs Ranitidine, cimetidine, famotidine, nizatidine Competitive inhibitors of H2-receptors on parietal and ECL cells Less potent than PPIs good safety profile- some available without prescription cimetidine may interfere with warfarin and phenytoin metabolism via cytochrome P450
PPI Omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole Irreversible inhibitors of H/K ATPase on parietal cell surface Potent acid suppression and rapid ulcer healing used in H. pylori therapy superior to H2 antagonists for healing ulcers and oesophagitis
Chelat Tripotassium dicitratobismuthate Ammoniacal suspension of complex bismuth salt anti-H. pylori activity and enhances mucosal protection May darken tongue and stools
C,Salts Sucralfate Aluminium salt of sucrose octasulphate little effect on acid -may protect ulcer base from peptic activity and enhance epithelial cell turnover Caution in renal impairment reports of bezoar formation
PGs Misoprostol Enhance mucosal blood flow, stimulate mucus and bicarbonate secretion stimulate epithelial proliferation Diarrhoea abortifacient-contraindicated in women of child-bearing age
27
PGE2
Gastrin
Histamine
Proglumide
ACh
H2
M3
Adenyl cyclase
Gastrin receptor
PGE receptor
ATP
cAMP
Ca
Ca
Protein Kinase (Activated)
K
H
K
Parietal cell
Proton pump
Lumen of stomach
Gastric acid
28
Surgery
  • The cure of most peptic ulcers by H. pylori
    eradication availability of safe, potent
    acid-suppressing drugs have made elective surgery
    for PUD a rare event

29
Complications
  • Perforation
  • Ggastric outlet obstruction
  • Bleeding

30
PEPTIC ULCER DISEASE IN OLD AGE
  • Gastroduodenal ulcers have a greater incidence,
    admission rate mortality.
  • Causes high prevalence of H. pylori NSAID use
    impaired defence mechanisms.
  • Atypical presentations pain dyspepsia are
    frequently absent or atypical so older people
    develop complications such as bleeding or
    perforation more frequently.
  • Bleeding older patients require more intensive
    management (including central venous pressure
    measurement) than younger patients because they
    tolerate hypovolaemic shock poorly.
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