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INTRODUCTION
 Group of disorder
characterized by the
presence of ulcer in any
portion of the GI tract
exposed to acid in
sufficient duration and
concentration.
 Discontinuity in the entire
thickness of the gastric or
duodenal mucosa that
persists as a result of acid
and pepsin in the gastric
juice.
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ETIOLOGY
 Helicobacter pylori, a type of bacteria that can cause a
stomach infection and inflammation.
 Frequent use of aspirin, Ibuprofen & other anti-
inflammatory drugs.
 Smoking
 Drinking too much of alcohol
 Radiation therapy
 Stomach cancer
 Stress.

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RISK FACTORS
 Taking NSAIDs
 Smoking
 Drinking too much of alcohol
 Stress.

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SIGNS

Complications
Weight loss
including ulcer
associated with
bleeding, perforation
nausea, vomiting
penetration or
and anorexia.
obstruction.

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SYMPTOMS

Abdominal Nocturnal
Heart burn
pain pain

Anorexia Nausea Vomiting Dyspepsia

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DIAGNOSIS
TEST FOR HELICOBACTER PYLORI
Endoscopic
Non endoscopic

Endoscopic
 Invasive
 More expensive
 Require 3 samples are taken from specific areas of the
stomach, as patchy distribution of false negative result.
certain medication may decrease the sensitivity of these
tests, antibiotic salts should be withheld for 4 weeks and
proton pump inhibitor for 1-2 week prior to endoscopic
testing.
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NON ENDOSCOPIC TEST
The non endoscopic test are;
o Tests that identify active infection.
o Test that detect antibodies
o Urea breath test
o Serologic antibody detection
o Stool antigen tests

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TREATMENT/MANAGEMENT
 To relieve symptoms
 To heal lesions
 To eradicate H. pylori infection
 To reduce morbidity
 To prevent complications
 Prevent recurrences.

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NON PHARMACOLOGICAL TREATMENT
 Patients with PUD should eliminate or reduce psychological
stress, cigarette smoking.
 Reduce the use of nonselective NSAIDs (including aspirin). If
possible, alternative agents such as acetaminophen, a non-
acetylated salicylate (e.g.,salsalate), or a COX-2 selective
inhibitor should be used for pain relief.
 Although there is no need for a special diet, patients should
avoid foods and beverages that cause dyspepsia or exacerbate
ulcer symptoms (e.g., spicy foods, caffeine, alcohol).

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TREATMENT ALGORITHM

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PHARMCOLOGICAL TREATMENT

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H2 RECEPTOR ANTAGONIST
 Ranitidine-150mg BD/300mg OD
 MOA: It acts by competitive reversible inhibitor of histamine on H2
receptor located on basolateral membrane of the parietal cells. also blocks
basal and postprandial acid secretion.
 ADR:On CNS-headache, dizziness, sedation
 On CVS-Bradycardia
PROTON PUMP INHIBITOR
 Omeprazole-20-40mg daily
 MOA :In acidic medium (pH less than 4) ionized into two cations like
sulfonamide and sulfenic acid. sulfenic acid irreversibily bind to H+K+
ATPase and inhibit proton pump.
 ADR: Antiandrogenic activity cause gynacomastic and erectile
dysfunction, headache, nausea, diarrhea or constipation, abdominal
discomfort, myalgia,
PROSTAGLANDIN ANALOGUE
 Misoprostol:PGE2 Synthetic analogue(dose;200mcg 4 times or 400mcg
2 times)
 MOA: Bind on EP3 receptor, inhibit gastrin release from G Cells, decrease
mucosal blood flow, promote bicarbonate secretion.
 ADR: Severe contraction, diarrhea, abdominal cramps, uterine bleeding
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ANTACIDS
 MOA: Neutralises acid in the stomach. Raise the antrum pH greater
than 4, rebound acidity to patients because pH Increases not acidic
condition.
 Systemic antacids: Sodium bicarbonate.
 Non systemic antacids: Aluminium hyroxide gel (250 mg)
 ADR: Acid rebounding.
ULCER PROTECTIVES
 Colloidal bismuth subcitrate, sucralfate.
 MOA: In acidic PH, Sucralfate undergoes polymerization and
assumes gel like consistency thus forms a coating over ulcer base.
Protein present on ulcer and dietary protein from food all coats an
ulcer base; protects from dangerous effects of acid and pepsin.
 DOSE: Sucralfate 1gm to be taken 1hour before the 3 meals and
before the bed time.
 ADR: Constipation, hypomagnesemia, rashes.
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SEQUENTIAL THERAPY
 This include the treatment with
 Amoxicillin 1000mg BD for a period of 1-5 days
 Standard doses of PPIs
&
 Clarithromycin 500 mg BD
 Metronidazole 500mg BD/ Tinidazole 500mg BD for a period
of 6-10 days.
 Standard doses of PPIs
 Chance of resistance is low, high successful rate for H. Pylori
eradication.
LEVOFLOXACIN BASED TRIPLE THERAPY
1. Levofloxacin 500mg BD
2. Amoxicillin 1000mg BD
3. Standard doses of PPI
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TREATMENT OF NSAID INDUCED ULCER

 Non selective NSAIDs should be discontinue (if possible) if an


active ulcer is confirmed. If the NSAID is stopped, most
uncomplicated ulcers will heal with standard regimens of an
H2RA, PPI, Sucralfate.

 PPIs are usually preferred because they provide more rapid ulcer
healing than H2RA or Sucralfate.

 If the NSAID must be continued in a patient despite ulceration,


consideration should be given to reducing the NSAID dose or
switching to acetaminophen, a non acetylated salicylate, a partially
selective COX-2 Inhibitor or a selective COX-2 Inhibitor.
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COMBINATION THERAPY
 Misoprostol co-therapy with a non selective NSAID
Misoprostol 200mcg & Diclofenac 50 or 75mg.
 H2 receptor antagonist with a non selective NSAID
 PPI co-therapy with a non selective NSAID.
 Selective Cox-2 inhibitors & partial Cox-2 inhibitors
TREATMENT FOR STRESS ULCER
 It include either oral or iv standard doses of PPI or
H2RA.

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TREATMENT FOR REFRACTORY ULCERS
 Ulcers are considered to be refractory to therapy when
symptoms, ulcers or both persist beyond 8 weeks (duodenal
ulcers) or 12 weeks (gastric ulcer) despite conventional
treatment or when several course of HP eradication fail.
 NSAID use, gastric acid hyper secretion, or tolerance to anti-
secretory effects of an H2RA may contribute to refractory
PUD.
 Patients with refractory ulcers should undergo upper endoscopy
to confirm non-healing ulcers, exclude malignancy, and assess
HP status.
 Maintenance therapy
 Surgery.

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