UPPER GI DISORDER II:

GASTRITIS
GASTRIC/DUODENAL ULCER
UPPER GI BLEEDING

BAMBANG SUTOPO
4 SEPTEMBER 2012
 Introduction
 Gastritis is the inflammation of the mucosa of
the stomach
 The mucosal response to injury involves
epithelial damage, mucosal inflammation, and
epithelial cell regeneration
 These separate processes often occur together,
but epithelial injury may be associated with
cellular regeneration without inflammation
 Classification Of Gastritis
Common Forms Uncommon Forms
 Acute Helicobacter pylori gastritis  Postantrectomy atrophic gastropathy

 Chronic Helicobacter pylori gastritis  Infectious gastritis

 Bacterial (other than Helicobacter pylori)
 Acute hemorrhagic and erosive
gastropathy - Helicobacter herlmannii
 Chronic chemical gastropathy
- Phlegmonous
- Mycobacterial
- Aspirin and other nonsteroidal
- Syphilitic
antiinflammatory drugs  Viral
- Bile reflux  Parasitic
- Others?  Fungal
 Metaplastic atrophic gastritis  Eosinophilic gastritis
- Autoimmune  Crohn’s disease

- Environmental  Sarcoidosis

 Chronic gastritis or gastropathy of  Isolated granulomatous gastritis

indeterminate type  Lymphocytic gastritis

 Hyperplastic gastropathies
 Ménétrier disease
 ZollingerEllison syndrome
 Most classifications distinguish acute, short-term
disease from chronic, long-term disease
 The terms acute and chronic are also used as
histopathologic descriptors
 acute inflammation denoting neutrophilic
inflammatory infiltration
 chronic inflammation refers to mononuclear
inflammatory cell infiltration, chiefly lymphocytes,
plasma cells, and macrophages
 Gastritis
 Acute gastritis often due to chemical injury
(alcohol, drugs), such as acute hemorrhagic and
erosive gastritis and acute H. pylori gastritis
 Chronic gastritis:
 Autoimmune (associated with vitamin B12
malabsorption (pernicious anaemia)
 Bacterial. Helicobacter pylori infection
 Chemical damage (bile reflux, drugs)
 Acute gastritis
 Drugs (non-steroidal
anti-inflammatory drugs
NSAID), alcohol cause
acute erosion (loss of
mucosa superficial to
muscularis mucosae).
Can result in severe
haemorrhage
 Acute Helicobacter
infection has a
prominent neutrophil
infiltrate
 Autoimmune chronic gastritis
 Autoantibodies to gastric parietal cells
 Hypochlorhydria/achlorhydria
 Loss of gastric intrinsic factor leads to
malabsorption of vitamin B12 with
macrocytic,megaloblastic anaemia
 Morphology of chronic gastritis
 Chronic inflammatory
cell infiltration
 Mucosal atrophy

 Intestinal (goblet cell)

metaplasia
Seen in Helicobacter and
autoimmune gastritis (not
chemical)
 Helicobacter pylori
 Adapted to live in
association with surface
epithelium beneath
mucus barrier
 Causes cell damage and
inflammatory cell
infiltration
 In most countries the
majority of adults are
infected
 Helicobacter gastritis
 Acute inflammation
mediated by
complement and
cytokines
 Polymorphisms
infiltrate epithelium and
may be partly
responsible for its
destruction
 An immune response is
also initiated (antibodies
may be detected in
serum)
 Helicobacter gastritis
 2 patterns of infection
 Diffuse involvement of body and antrum
(“pan gastritis” associated with diminishing
acid output)
 Infection confined to antrum (antral gastritis,
associate with increased acid output)
 Chemical gastritis
 Commonly seen with
bile reflux (toxic to
cells)
 Prominent
hyperplastic response
(inflammatory cells
scanty)
 With time –
intestinal metaplasia
 Clinical manifestation
 Upper abdominal complaints (i.e., dyspepsia or
indigestion) are encountered with a prevalence
of 13% to 27% in adults
 Nonulcer dyspepsia, when clinical evaluation
reveals no organic cause (e.g., peptic ulcer,
gastric cancer, esophagitis, cholelithiasis)
 In its chronic phase, H pylori gastritis is not
regularly associated with characteristic
symptoms or endoscopic findings.
 Clinical manifestation, cont
 Epigastric discomfort
 Anorexia
 Nausea and vomitus
 ASA induced- may have dyspepsia
 May have hemorrhage
 With food poisoning may have severe symptoms
within 5 hours of ingestion of bacteria
 Diagnosis
 For definitive diagnosis of type must have
endoscopy with biopsy
 A complete blood count may show anemia
 Stool for occult blood
 Gastric analysis for HCl acid
 Cytologic exam to exclude gastric cancer
 Interventions
 Treat symptoms
 Remove cause
 With bleeding may require blood transfusion
 Replace fluids
 Surgery if conservative measure don’t work
(i.e. partial gastrectomy)
 Drug therapy
RELIEF SYMPTOM:
ANTACID
PROKINETIC
SPASMOLYTIC

SUPPRESS ACID:
RANITIDIN, FAMOTIDIN, CIMETIDIN, PROTON PUMP INHIBITOR

ERADICATION OF H PYLORI:
PPI + CLARITHOMYCIN + AMOXYCILLINE/METRONIDAZOLE

PATIENTS WITH CHR GASTRITIS MAY REQUIRE VIT B12

 Education
 About cause:
 Medication – steroid, chemo, ASA, NSAIDS
 Diet –limited tea, coffee, hot spices, alcohol,
smoking
 Stress reduction- relaxation techniques, distraction