ACID PEPTIC DISORDERS

Dr. K. George Thomas . MD.DM

www.similima.comPushpagiri Medical College, Tiruvalla 1
Dept of Gastroenterology,

Dyspepsia
A common disorder with a negative impact
on patients quality of life .

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Dyspepsia

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DYSPEPSIA
Constellation of symptoms

Rome II criteria : persistent or recurrent abdominal

pain or abdominal discomfort centered in the upper
abdomen

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Dyspepsia
Dyspepsia : categorized
Uninvestigated : new onset / recurrent

no causes found
Functional dyspepsia : undergone tests

no causes found
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GERD
Any symptomatic condition resulting from

episodes of GE reflux or histopathologic

alteration

Reflux esophagitis is a condition experienced by

a subset of GERD pts with endoscopic evidence

of mucosal lesions
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Peptic ulcer
Excavated defects / holes in the GI mucosa

Results from damage to epithelial cells due to

effects of acid and pepsin

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Peptic ulcer - sites

Common in stomach, duodenum or both

Any part of GIT exposed to acid and pepsin

in sufficient concentration / duration

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Peptic ulcer
Incidence : 10 % of population
DU GU -

M:F- 5:1
M : F - 2 : 1 / 1:1

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Etiology
H pylori
NSAIDs
Smoking
Acid pepsin vs. mucosal resistance
Diet / other diseases / genetics / emotional stress

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Acid pepsin vs mucosal resistance

acid

pH
+2

pepsin

H CO 3

Blood flow

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Helicobacter pylori
Slow growing, microaerophilic, motile , gram neg

spiral flagellated bacterial organism

Discovered by Robin Warren & Barry Marshall

from Australia 1981, won Nobel Prize

80 % DU

60% GU
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Hp : pathogenesis
Localizes in mucosal layer, adherent to epithelial

surface of gastric mucosa only

Produces urease NH3 from urea pH around

bacteria (ammonia cloud)

Releases cytotoxins inflammation ulcer
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DU sequence
4

Gastric metaplasia

H Cl secretion
Gastrin release from
gastrin cells

Inflammn /ulceration

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Antral gastritis

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GU sequence

Gastric mucosal resistance to attack by H Cl

1% pan gastritis proliferation of bacteria

mutagenic nitrites from nitrates in food Ca

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Diagnosis
1.

Non invasive

Serology
Urea breath test

2.

Invasive

Histology
Urease test
Culture
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NSAIDS
Causative in 30 % GU, less of DU
Interference with PG E levels impaired cyto protection
Increased risk of complications

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PG pathway
Phospho lipid
Arachidonic acid
Cox 1

Cox 2
NSAIDS

House keeping

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inflammatory

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Smoking
Increases Hcl output
Decreases PG levels
Decreases bicarbonate levels

Increases risk of GU > DU

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Pathology
GU - single, lesser curve, antrum-body jn
DU - D1 50% on anterior wall
GU + DU : 10%
> 1 Ulcer :10%
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Clinical features
1. Spontaneous remissions / relapses
1. Long standing
1. Hallmarks

Location
Episodic
Relationship to food

4 . Vomiting < 40% - persistent vomiting ?GOO

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Clinical features
5. Atypical symptoms

elderly
NSAIDS

6. Silent
7 . Complications

bleeding , penetration,
perforation , obstruction

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Investigations
UGI endoscopy

Oesophago gastro duodenosopy [ OGD]

Gastroscopy

[Barium studies ]
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Treatment- Aims
Relief of symptoms
Heal ulcer
Prevent complications
Prevent recurrence
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General measures
Stop smoking
Avoid NSAIDs, alcohol
Dietary modifications ?
Treat / avoid stress
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Treatment
Antacids
H2 receptor blockers

Ranitidine
Famotidine
Proton Pump Inhibitors [ PPI ]
Omeprazole

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Esomeprazole
Lansoprazole
Pantoprazole
Rabeprazole

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Treatment
Ancillary : Prokinetics

Metoclopramide
Domperidone
Cisapride
Mosapride
Itopride
Levosulpiride
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Mainstay of treatment
H pylori eradication
Multiple drugs
Triple drugs x 14 days

PPI / Clarithromycin / Amoxycillin

Quadruple
Bismuth
Sequential therapy
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Indication for eradication of Hp

All Hp + ulcers
All cases of Ca stomach Hp +
Relatives of Hp + Ca pts
Prophylactic in a pt to be on long term NSAIDs
Gastric maltoma
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Hp eradication

No use in Non ulcer dyspepsia

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Surgical treatment
Emergency

bleeding
perforation
Elective

complications - GOO
failure of medical treatment
recurrent ulcer
GJ / partial gastrectomy / HSV- ssv / Pyloroplasty
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GERD
Any symptomatic condition resulting from episodes

of GE reflux or histopathologic alteration

Reflux esophagitis is a condition experienced by a

subset of GERD pts with endoscopic evidence of

mucosal lesions

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GERD -Epidemiology

7% of western population daily , 15 % weekly

Asians less symptomatic, less complications

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GERD- Pathophysiology
TLESR - Transient Lower Esophageal Sphincter

Relaxation
Hypotensive lower esophageal sphincter
Hiatus hernia
Delayed gastric emptying
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Clinical features
Typical:

Heart burn
Regurgitation
Dysphagia

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Atypical
Laryngitis- hoarseness,post laryngeal edema,

vocal cord granuloma

Asthma
Chronic cough [10-40% of chronic cough, 50 % have

no GERD symptoms]

Vagally mediated esophago bronchial reflex

Nocturnal / post prandial symptoms
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Differential diagnosis
Peptic ulcer
Non ulcer dyspepsia
Biliary colic
Motility disorders
Coronary artery disease
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Investigations
UGI Endoscopy
Esophageal pH metry ambulatory , 24 hr
Therapeutic trial with PPI

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Treatment
Lifestyle modifications
Head end elevation
Avoid tight clothes
Weight reduction
Diet - fat, quantity, avoid recumbency
Alcohol, smoking
Drugs
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Drug therapy
H2RA
PPI
Prokinetics

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Treatment
Endoscopic:

Radiofrequency ablation
Endoscopic suturing
Injection of inert drugs

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Treatment- surgery
Fundoplication
Laparoscopic antireflux surgery

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Complications
Peptic stricture
Barretts esophagus

**
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