gastritis
DESCRIPTION
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Gastritis
dr. Isbandiyah, SpPD
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Anatomical site
ANTRUM
CARDIA
BODY
MUCOUS SECRETING cells
SPECIALISED SECRETORY PARIETAL - ACIDCHIEF -
PEPSINOGEN ENDOCRINEHIST,
SOMASTATIN
MUCOUS SECRETING ENDOCRINE :GASTRIN, 5HT
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Definition
• The term gastritis is used to denote inflammation associated with mucosal injury
• Gastritis is mostly a histological term that needs biopsy to be confirmed
• Gastritis is usually due to infectious agents (such as Helicobacter pylori) and autoimmune and hypersensitivity reactions.
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Causes H pylori (most common cause of ulceration) NSAIDs, aspirin Gastrinoma (Zollinger-Ellison syndrome) Severe stress (eg, trauma, burns), Curling ulcers Alcohol Bile reflux Pancreatic enzyme reflux Radiation Staphylococcus aureus exotoxin Bacterial or viral infection
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Pathophysiology The mechanisms of mucosal injury in gastritis are thought to be
an imbalance of aggressive factors
• acid production or pepsin
and defensive factors• mucus production • bicarbonate • and blood flow
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FAKTOR DEFENSIF
FAKTOR AGRESIF
“IMBALANCE”
Robbins.Pathology Anatomy
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Pathogenesis
• In normal acid/pepsin attack is balanced by mucosal defences
• Increased attack by hyperacidity
• Weakened mucosal defence – the major factor (H. pylori related)
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Patients typically present with abdominal pain that has
the following characteristics
Epigastric to left upper quadrant
Frequently described as burning
May radiate to the back
Usually occurs 1-5 hours after meals
May be relieved by food, antacids (duodenal), or vomiting (gastric)
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Treatment
• Drugs:– Antasid– Antagonis reseptor H2– proton pump inhibitor– Antikolinergic– Sitoprotektor sukralfat dan rebamipid– prostaglandin
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Chronic gastritis
• A – autoimmune• B – bacterial (helicobacter)• C - chemical
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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
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Morphology of chronic gastritis
• Chronic inflammatory cell infiltration
• Mucosal atrophy• Intestinal (goblet cell)
metaplasia
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Chemical gastritis
• Commonly seen with bile reflux (toxic to cells)
• Prominent hyperplastic response (inflammatory cells scanty)
• With time – intestinal metaplasia
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Helicobacter pylori
• Causes cell damage and inflammatory cell infiltration
• In most countries the majority of adults are infected
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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)
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Diagnostic test for H. Pilori infection
• Non endoscopic– Serologic test– Urea breath test (UBT)– Fecal antigen test
• Endoscopic– Urease based test (CLO)– Histologic assessment– Cultur
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Tretment regimens for H. pilori infection
• Standart triple drug regimen– PPI + claritomycin + amoxicillin or metronidazole
• Sequential therapy for initial treatment– PPI + amoxicillin for 5 d followed by PPI +
claritomycin + metronidazole for 5 d
• Second line regimen for failed initial treatment– PPI + bismuth +tetracycline + metronidazole
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Terapi Eradikasi H.Pylori
• PPI 2x1+ amoksisilin 2x1000 mg + klaritromisin 2x500 mg
• PPI 2x1 + metronidazol 3x500 mg + klaritromisin 2x500 mg
• PPI 2x1 + metronidazol 3x500 mg + amoksisilin 2x1000 mg
• PPI 2x1 + metronidazol 3x500 mg + tetrasiklin 4x500 mg
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•Regulation of gastric acid secretion